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| 1 | Case study on the first immigration of fall armyworm,Spodoptera frugiperda invading into China显示文摘The fall armyworm(FAW),Spodoptera frugiperda is one of the most damaging crop pests,and it has become major threat to the food security of many countries.In order to monitor possible invasion of this pest into China,a searchlight trap was established in March 2018 in western Yunnan Province,China,where it has served as the'first station'for many pests that have migrated from Myanmar to China.A number of suspected FAW moths were captured and identified by DNA sequencing.The results showed that the FAW moth was first captured on December 11 and formed its first immigration peak in mid-December 2018.DNA detection revealed that the early invading FAW population was the'corn-strain'.The field survey indicated that the pest mainly colonized corn in Pu’er,Dehong and Baoshan areas.Migration trajectory simulation implied that the moths might have mainly come from the eastern area in the mid-latitude region of Myanmar(20-25°N,94-100°E).This case study confirmed the first immigration of FAW into China,and will be helpful for guiding monitoring and management work to control this pest. | SUN Xiao-xu HU Chao-xing JIA Hui-ru WU Qiu-lin SHEN Xiu-jing ZHAO Sheng-yuan JIANG Yu-ying WU Kong-ming | 2021 | Journal of Integrative Agriculture2021，20，3： | 66 |
| 2 | Management of hepatocellular carcinoma with portal vein tumor thrombosis: Review and update at 2016显示文摘Portal vein tumor thrombosis(PVTT) is a common phenomenon in hepatocellular carcinoma(HCC). Compared to HCC without PVTT, HCC with PVTT is characterized by an aggressive disease course, worse hepatic function, a higher chance of complications related to portal hypertension and poorer tolerance to treatment. Conventionally, HCC with PVTT is grouped together with metastatic HCC during the planning of its management, and most patients are offered palliative treatment with sorafenib or other systemic agents. As a result, most data on the management of HCC with PVTT comes from subgroup analyses or retrospective series. In the past few years, there have been several updates on management of HCC with PVTT. First, it is evident that HCC with PVTT consists of heterogeneous subgroups with different prognoses. Different classifications have been proposed to stage the degree of portal vein invasion/thrombosis, suggesting that different treatment modalities may be individualized to patients with different risks. Second, more studies indicate that more aggressive treatment, including surgical resection or locoregional treatment, may benefit select HCC patients with PVTT. In this review, we aim to discussthe recent conceptual changes and summarize the data on the management of HCC with PVTT. | Stephen L Chan Charing CN Chong Anthony WH Chan Darren MC Poon Kenneth SH Chok | 2016 | World Journal of Gastroenterology2016，22，32： | 44 |
| 3 | Endoscopic and surgical resection of T1a/T1b esophageal neoplasms: A systematic review显示文摘AIM: To investigate potential therapeutic recommendations for endoscopic and surgical resection of T1a/ T1b esophageal neoplasms. METHODS: A thorough search of electronic databases MEDLINE, Embase, Pubmed and Cochrane Library, from 1997 up to January 2011 was performed. An analysis was carried out, pooling the effects of outcomes of 4241 patients enrolled in 80 retrospective studies. For comparisons across studies, each reporting on only one endoscopic method, we used a random effects meta-regression of the log-odds of the outcome of treatment in each study. 'Neural networks' as a data mining technique was employed in order to establish a prediction model of lymph node status in superficial submucosal esophageal carcinoma. Another data mining technique, the 'feature selection and root cause analysis', was used to identify the most impor-tant predictors of local recurrence and metachronous cancer development in endoscopically resected patients, and lymph node positivity in squamous carcinoma (SCC) and adenocarcinoma (ADC) separately in surgically resected patients. RESULTS: Endoscopically resected patients: Low grade dysplasia was observed in 4% of patients, high grade dysplasia in 14.6%, carcinoma in situ in 19%, mucosal cancer in 54%, and submucosal cancer in 16% of patients. There were no significant differences between endoscopic mucosal resection and endoscopic submucosal dissection (ESD) for the following parameters: complications, patients submitted to surgery, positive margins, lymph node positivity, local recurrence and metachronous cancer. With regard to piecemeal resection, ESD performed better since the number of cases was significantly less [coefficient: -7.709438, 95%CI: (-11.03803, -4.380844), P < 0.001]; hence local recurrence rates were significantly lower [coefficient: -4.033528, 95%CI: (-6.151498, -1.915559),P < 0.01]. A higher rate of esophageal stenosis was observed following ESD [coefficient: 7.322266, 95%CI: (3.810146, 10.83439), P < 0.001]. A significantly greater number of SCC patients were submitted to surgery (log-odds, ADC: -2.1206 ± 0.6249 vs SCC: 4.1356 ± 0.4038, P < 0.05). The odds for re-classification of tumor stage after endoscopic resection were 53% and 39% for ADC and SCC, respectively. Local tumor recurrence was best predicted by grade 3 differentiation and piecemeal resection, metachronous cancer development by the carcinoma in situ component, and lymph node positivity by lymphovascular invasion. With regard to surgically resected patients: Significant differences in patients with positive lymph nodes were observed between ADC and SCC [coefficient: 1.889569, 95%CI: (0.3945146, 3.384624), P<0.01). In contrast, lymphovascular and microvascular invasion and grade 3 patients between histologic types were comparable, the respective rank order of the predictors of lymph node positivity was: Grade 3, lymphovascular invasion (L+), microvascular invasion (V+), submucosal (Sm) 3 invasion, Sm2 invasion and Sm1 invasion. Histologic type (ADC/SCC) was not included in the model. The best predictors for SCC lymph node positivity were Sm3 invasion and (V+). For ADC, the most important predictor was (L+). CONCLUSION: Local tumor recurrence is predicted by grade 3, metachronous cancer by the carcinoma insitu component, and lymph node positivity by L+. T1b cancer should be treated with surgical resection. | George Sgourakis Ines Gockel Hauke Lang | 2013 | World Journal of Gastroenterology2013，19，9： | 40 |
| 4 | Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion显示文摘AIM:To investigate the role of hepatocyte growth factor(HGF) in cholangiocarcinoma(CCA) cell invasiveness and the mechanisms underlying such cellular responses. METHODS:Effects of HGF on cell invasion and motility were investigated in two human CCA cell lines,HuCCA-1 and KKU-M213,using Transwell in vitro assay.Levels of proteins of interest and their phosphorylated forms were determined by Western blotting.Localization of E-cadherin was analyzed by immunofluorescence staining and visualized under confocal microscope. Activities of matrix degrading enzymes were determined by zymography. RESULTS:Both CCA cell lines expressed higher Met levels than the H69 immortalized cholangiocyte cell line.HGF induced invasion and motility of the cell lines and altered E-cadherin from membrane to cytoplasm localization,but did not affect the levels of secreted matrix metalloproteinase(MMP) -2,MMP-9 andurokinase plasminogen activator,key matrix degrading enzymes involved in cell invasion.Concomitantly,HGF stimulated Akt and extracellular signal-regulated kinase(ERK) 1/2 phosphorylation but with slightly different kinetic profiles in the two cell lines.Inhibition of the phosphoinositide 3-kinase(PI3K) /Akt pathway by the PI3K inhibitor,LY294002,markedly suppressed HGFstimulated invasion of both CCA cell lines,and inhibition of the ERK pathway by U0126 suppressed HGF-induced invasion of the KKU-M213 cell line but had a moderate effect on HuCCA-1 cells. CONCLUSION:These data indicate that HGF promotes CCA cell invasiveness through dys-localization of E-cadherin and induction of cell motility by distinct signaling pathways depending on cell line type. | Apaporn Menakongka Tuangporn Suthiphongchai | 2010 | World Journal of Gastroenterology2010，16，6： | 33 |
| 5 | Relationship between expression of CD44v6 and nm23-H1 and tumor invasion and metastasis in hepatocellular carcinoma显示文摘INTRODUCTIONCD44isacelsurfacetransmembraneglycoprotein.Asakindofadhesivemolecule,itparticipatesincelcelandcelmatrixadhesion... | XIAO Cheng Zhi, DAI Yi Min, YU Hong Yu, WANG Jian Jun and NI Can Rong | 1998 | World Journal of Gastroenterology1998，4，5： | 23 |
| 6 | CD97 promotes gastric cancer cell proliferation and invasion through exosome-mediated MAPK signaling pathway显示文摘AIM: To investigate the mechanism underlying the promoting role of CD97 in gastric cancer cell proliferation and invasion. METHODS: Two types of exosomes released by gastric cancer cells with high(SGC/wt) or low(SGC/kd) CD97 expression were isolated by ultracentrifugation and identified by electron microscopy and western blot analysis. The influences of the two exosomes on gastric cancer cell proliferation and invasion were investigated by proliferation and Matrigel invasion assays. Exosomal mi RNAs were subsequently isolated from the two samples and their mi RNA profiles were compared via microarray assay analysis. Reverse transcriptionquantitative real-time polymerase chain reaction was used to validate the microarray assay. Target genes of the differently expressed micro RNAs were predicted based on five independent algorithms and were then subjected to gene oncology enrichment and Kyoto encyclopedia of genes and genomes(KEGG) pathway analysis. After identifying the pathway that was the most likely altered, tumor cells were treated with the two exosomes at different concentrations, and the pathway activation was identified through western blot analysis.RESULTS: Exosomes isolated from SGC/wt cells significantly promoted tumor cell proliferation in a dose-dependent manner in vitro. SGC/wt exosomesalso significantly elevated the invasiveness of both SGC/wt(129.67 ± 8.327 vs 76.00 ± 5.292, P < 0.001) and SGC/kd(114.52 ± 9.814 vs 45.73 ± 4.835, P < 0.001) cells as compared to the exosomes released by SGC/kd cells. Microarray assay of the two exosomes revealed that 62 mi RNAs were differently regulated with a signal intensity of > 500 and a false discovery rate < 0.05. The following KEGG analysis defined the MAPK signaling pathway as the most likely candidate pathway that regulated tumor cell proliferation and invasion. Through western blot analysis, significant up-regulations of phosphorylated MAPKs, including extracellular signal-regulated kinase, Jun NH2-terminal kinase, and p38 mitogen-activated protein kinase, were detected in a dose-dependent manner in the SGC/wt exosomes treated groups, confirming activation of the MAPK signaling pathway stimulated by SGC/wt exosomes.CONCLUSION: CD97 promotes gastric cancer cell proliferation and invasion in vitro through exosomemediated MAPK signaling pathway, and exosomal mi RNAs are probably involved in activation of the CD97-associated pathway. | Chao Li Da-Ren Liu Guo-Gang Li Hou-Hong Wang Xiao-Wen Li Wei Zhang Yu-Lian Wu Li Chen | 2015 | World Journal of Gastroenterology2015，21，20： | 22 |
| 7 | Dihydromyricetin inhibits migration and invasion of hepatoma cells through regulation of MMP-9 expression显示文摘AIM:To investigate the effects of dihydromyricetin(DHM)on the migration and invasion of human hepatic cancer cells.METHODS:The hepatoma cell lines SK-Hep-1 and MHCC97L were used in this study.The cells were cultured in RPIM-1640 medium supplemented with 10%fetal bovine serum at 37℃in a humidified 5%CO2incubator.DHM was dissolved in dimethyl sulfoxide and diluted to various concentrations in medium before applying to cells.MTT assays were performed to measure the viability of the cells after DHM treatment.Wound healing and Boyden transwell assays were used to assess cancer cell motility.The invasive capacity of cancer cells was measured using Matrigel-coated transwell chambers.Matrix metalloproteinase(MMP)-2/9 activity was examined by fluorescence analysis.Western blot was carried out to analyze the expression of MMP-2,MMP-9,p-38,JNK,ERK1/2 and PKC-δproteins.All data were analyzed by Student’s t tests in GraphPad prism 5.0software and are presented as mean±SD.RESULTS:DHM was found to strongly inhibit the migration of the hepatoma cell lines SK-Hep-1(without DHM,24 h:120±8μmol/L vs 100μmol/L DHM,24h:65±10μmol/L,P<0.001)and MHCC97L(without DHM,24 h:126±7μmol/L vs 100μmol/L DHM,24h:74±6μmol/L,P<0.001).The invasive capacity of the cells was reduced by DHM treatment(SK-Hep-1cells without DHM,24 h:67±4μmol/L vs 100μmol/L DHM,24 h:9±3μmol/L,P<0.001;MHCC97L cells without DHM,24 h:117±8μmol/L vs 100μmol/L DHM,24 h:45±2μmol/L,P<0.001).MMP2/9 activity was also inhibited by DHM exposure(SK-Hep-1 cells without DHM,24 h:600±26μmol/L vs 100μmol/L DHM,24 h:100±6μmol/L,P<0.001;MHCC97L cells without DHM,24 h:504±32μmol/L vs 100μmol/L DHM 24 h:156±10μmol/L,P<0.001).Western blot analysis showed that DHM decreased the expression level of MMP-9 but had little effect on MMP-2.Further investigation indicated that DHM markedly reduced the phosphorylation levels of p38,ERK1/2 and JNK in a concentration-dependent manner but had no impact on the total protein levels.In addition,PKC-δprotein,a key protein in the regulation of MMP family protein expression,was up-regulated with DHM treatment.CONCLUSION:These findings demonstrate that DHM inhibits the migration and invasion of hepatoma cells and may serve as a potential candidate agent for the prevention of HCC metastasis. | Qing-Yu Zhang Ran Li Guo-Fang Zeng Bin Liu Jie Liu Yang Shu Zhong-Kao Liu Zhi-Dong Qiu Dong-Jun Wang Hui-Lai Miao Ming-Yi Li Run-Zhi Zhu | 2014 | World Journal of Gastroenterology2014，20，29： | 23 |
| 8 | Long noncoding RNA LINC00520 prevents the progression of cutaneous squamous cell carcinoma through the inactivation of the PI3K/Akt signaling pathway by downregulating EGFR显示文摘Background: Long noncoding RNAs (lncRNAs) play pivotal roles in various malignant tumors. Epidermal growth factor receptor (EGFR) signaling is associated with the pathogenesis of cutaneous squamous cell carcinoma (cSCC). This study aimed to explore the role of LINC00520 in the development of cSCC via EGFR and phosphoinositide 3-kinase-protein kinase B (PI3K/Akt) signaling pathways. Methods: A microarray analysis was applied to screen differentially expressed lncRNAs in cSCC samples. The A431 cSCC cell line was transfected and assigned different groups. The expression patterns of LINC00520, EGFR, and intermediates in the PI3K/Akt pathway were characterized using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting analysis. Cell proliferation, migration, and invasion were detected using the MTT assay, scratch test, and Transwell assay, respectively. Cell-based experiments and a tumorigenicity assay were conducted to assess the effect of LINC00520 on cSCC progression. This study was ended in September 2017. Comparisons between two groups were analyzed with t-test and comparisons among multiple groups were analyzed using one-way analysis of variance. The nonparametric Wilcoxon rank sum test was used to analyze skewed data. The enumerated data were analyzed using the chi-square test or Fisher exact test. Results: Data from chip GSE66359 revealed depletion of LINC00520 in cSCC. Cells transfected with LINC00520 vector and LINC00520 vector + si-EGFR showed elevated LINC00520 level but decreased levels of the EGFR, PI3K, AKT, VEGF, MMP-2 and MMP-9 mRNAs and proteins, and inhibition of the growth, migration and adhesion of cSCC cells, while the si-LINC00520 group showed opposite trends (all P < 0.05). Compared with the LINC00520 vector group, the LINC00520 vector + si-EGFR group showed decreased levels of the EGFR, PI3K, AKT, VEGF, MMP-2 and MMP-9 mRNAs and proteins, and inhibition of the growth, migration and adhesion of cSCC cells, while the LINC00520 vector+ EGFR vector group showed opposite results (all P < 0.05). Conclusion: Based on our results, LINC00520-targeted EGFR inhibition might result in the inactivation of the PI3K/Akt pathway, thus inhibiting cSCC development. | Xue-Ling Mei Shah Zhong | 2019 | Chinese Medical Journal2019，，4： | 20 |
| 9 | Inhibition of long non-coding RNA TUG1 on gastric cancer cell transference and invasion through regulating and controlling the expression of miR-144/c-Met axis显示文摘Objective: To discuss the expression of long noncoding RNA TUG1(lnc RNA-TUG1) in gastric carcinoma(GC) and its effects on the transferring and invading capacity of gastric carcinoma cells. Methods: Forty cases of carcinoma tissue and para-carcinoma tissue were selected from GC patients who underwent surgical removal in Zhejiang Provincial Hospital of Chinese Traditional Medicine and Wenzhou Central Hospital from January, 2013 to December, 2014; the expressing level of lnc RNA-TUG1 in GC and para-C tissues was detected by applying the q RT-PCR technique. The correlation between lnc RNA-TUG1 expression and patients' clinical data was classified and analyzed. SGC-7901 cells were transfected using lnc RNA-TUG1 specific si RNA. Changes of the transferring and invading capacity of si RNAtransfected SGC-7901 cells were scratch-tested and transwell-detected. q RT-PCR was applied to detect the expression level of micro RNA-144 after lnc RNA-TUG1 was silenced. Changes of c-Met m RNA and protein expressions was detected by q RT-PCR and western-blot test. Results: The expression level of lnc RNA-TUG1 in GC tissue was significant higher than that in para-C tissue(P<0.05) and the high expression level of lnc RNA-TUG1 in GC tissue was significantly correlated with tumor lymph nodes metastasis and advance TNM phasing(P<0.05). The transferring and invading capacity of SGC-7901 cells was highly inhibited after being transfected by lnc RNA-TUG1 specific si RNA(P<0.05). The results of q RT-PCR and western-blot proved that the expression of micro RNA-144 was significantly boosted and the expression level of c-Met m RNA and protein was inhibited after lnc RNA-TUG1 was silenced(P<0.05). Conclusions: lnc RNA-TUG1 shows an up-regulated expression in GC tissue and that bears a correlation with clinicopathological features of malignant tumor. lnc RNATUG1 can promote the transferring and invading capacity of GC by inhibiting the pathway of micro RNA-144/c-Met. | Ting-Ting Ji Xuan Huang Jie Jin Sheng-Hua Pan Xiao-Ju Zhuge | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，5： | 20 |
| 10 | miR-21 targets and inhibits tumor suppressor gene PTEN to promote prostate cancer cell proliferation and invasion:An experimental study显示文摘Objective: To study whether miR-21 targets and inhibits tumor suppressor gene PTEN can promote prostate cancer cell proliferation and invasion,Methods: Prostate cancer cell lines PC-3 were cultured and divided into negative control group(NC group),miR-21 group,pc DNA3.1 group,miR-21+pc DNA3.1 group and miR-21+PTEN group that were transfected with different mi R and plasmid,respectively,After 12 h and 24 h of transfection,the cell viability and invasive cell number were determined; after 24 h of transfection,Bcl-2,Survivin,MMP2,MMP9,PTEN,PI3 K,and AKT expression in cells were determined,Results: After 12 h and 24 h of transfection,OD value and invasive cell number of miR-21 group were significantly higher than those of NC group; after 24 h of transfection,Bcl-2,Survivin,MMP2,MMP9,PI3 K and AKT expression levels were significantly higher than those of NC group while PTEN expression level was significantly lower than that of NC group; after 12 h and 24 h of transfection,OD value and invasive cell number of mi R-21+pcDNA3.1 group were significantly higher than those of pc DNA3.1 group,and the OD value and invasive cell number of mi R-21+PTEN group were significantly lower than those of mi R-21+pcDNA3.1 group; after 24 h of transfection,Bcl-2,Survivin,MMP2 and MMP9 content of mi R-21+pc DNA3.1 group were significantly higher than those of pcDNA3.1 group,and Bcl-2,Survivin,MMP2 and MMP9 content of miR-21+PTEN group were significantly lower than those of mi R-21+pcDNA3.1 group,Conclusions: miR-21 can target and inhibit tumor suppressor gene PTEN expression to promote prostate cancer cell proliferation and invasion. | Yu Yang Jia-Xiang Guo Zhi-Qiang Shao | 2017 | Asian Pacific Journal of Tropical Medicine2017，10，1： | 20 |
| 11 | Astragaloside Ⅳ inhibits pathological functions of gastric cancer-associated fibroblasts显示文摘AIM To investigate the inhibitory effect of astragaloside IV on the pathological functions of cancer-associated fibroblasts,and to explore the underlying mechanism.METHODS Paired gastric normal fibroblast(GNF) and gastric cancer-associated fibroblast(GCAF) cultures were established from resected tissues. GCAFs were treated with vehicle control or different concentrations of astragaloside Ⅳ. Conditioned media were prepared from GNFs,GCAFs,control-treated GCAFs,and astragaloside Ⅳ-treated GCAFs,and used to culture BGC-823 human gastric cancer cells. Proliferation,migration and invasion capacities of BGC-823 cells were determined by MTT,wound healing,and Transwell invasion assays,respectively. The action mechanism of astragaloside Ⅳ was investigated by detecting the expression of micro RNAs and the expression and secretion of the oncogenic factor,macrophage colonystimulating factor(M-CSF),and the tumor suppressive factor,tissue inhibitor of metalloproteinase 2(TIMP2),in different groups of GCAFs. The expression of the oncogenic pluripotency factors SOX2 and NANOG in BGC-823 cells cultured with different conditioned media was also examined.RESULTS GCAFs displayed higher capacities to induce BGC-823 cell proliferation,migration,and invasion than GNFs(P < 0.01). Astragaloside Ⅳ treatment strongly inhibited the proliferation-,migration-and invasion-promoting capacities of GCAFs(P < 0.05 for 10 μmol/L,P < 0.01 for 20 μmol/L and 40 μmol/L). Compared with GNFs,GCAFs expressed a lower level of micro RNA-214(P < 0.01) and a higher level of micro RNA-301 a(P < 0.01). Astragaloside Ⅳ treatment significantly upregulated micro RNA-214 expression(P < 0.01) and down-regulated micro RNA-301 a expression(P < 0.01) in GCAFs. Reestablishing the micro RNA expression balance subsequently suppressed M-CSF production(P < 0.01) and secretion(P < 0.05),and elevated TIMP2 production(P < 0.01) and secretion(P < 0.05). Consequently,the ability of GCAFs to increase SOX2 and NANOG expression in BGC-823 cells was abolished by astragaloside Ⅳ.CONCLUSION Astragaloside Ⅳ can inhibit the pathological functions of GCAFs by correcting their dysregulation of micro RNA expression,and it is promisingly a potent therapeutic agent regulating tumor microenvironment. | Zhen-Fei Wang Da-Guang Ma Zhe Zhu Yong-Ping Mu Yong-Yan Yang Li Feng Hao Yang Jun-Qing Liang Yong-Yan Liu Li Liu Hai-Wen Lu | 2017 | World Journal of Gastroenterology2017，23，48： | 15 |
| 12 | Systematic review of prognostic importance of extramuralvenous invasion in rectal cancer显示文摘AIM: To systematically review the survival outcomes relating to extramural venous invasion in rectal cancer.METHODS: A systematic review was conducted using PRISMA guidelines. An electronic search was carried out using MEDLINE, EMBASE, CINAHL, Cochrane library databases, Google scholar and Pub Med until October 2014. Search terms were used in combination to yield articles on extramural venous invasion in rectal cancer. Outcome measures included prevalence and 5-year survival rates. These were graphically displayed using Forest plots. Statistical analysis of the data was carried out.RESULTS: Fourteen studies reported the prevalence of extramural venous invasion(EMVI) positive patients. Prevalence ranged from 9%-61%. The pooled prevalence of EMVI positivity was 26% [Random effects: Event rate 0.26(0.18, 0.36)]. Most studies showed that EMVI related to worse oncological outcomes. The pooled overall survival was 39.5% [Random effects: Event rate 0.395(0.29, 0.51)].CONCLUSION: Historically, there has been huge variation in the prevalence of EMVI through inconsistent reporting. However the presence of EMVI clearly leads to worse survival outcomes. As detection rates become more consistent, EMVI may be considered as part of risk-stratification in rectal cancer. Standardised histopathological definitions and the use of magnetic resonance imaging to identify EMVI will improve detection rates in the future. | Manish Chand Muhammed RS Siddiqui Ian Swift Gina Brown | 2016 | World Journal of Gastroenterology2016，22，4： | 15 |
| 13 | 肝细胞癌合并血管侵犯专家共识(讨论稿)显示文摘肝细胞癌合并血管侵犯是影响肝细胞癌预后的重要因素。血管侵犯分为大血管侵犯(macrovascular invasion)和微小血管侵犯(microvascular invasion,以下简称m VI)。大血管侵犯指门静脉及其主要分支形成的癌栓(portal vein tumor thrombus,以下简称PVTT)。而m VI尚无明确统一定义,多指癌栓位于门静脉终末分支(portal radicle vein)。 | | 2015 | 肝癌电子杂志2015，2，3： | 15 |
| 14 | Propofol inhibits the adhesion of hepatocellular carcinoma cells by upregulating microRNA-199a and downregulating MMP-9 expression显示文摘BACKGROUND: Propofol is one of the extensively and commonly used intravenous anesthetics and has the ability to influence the proliferation, motility, and invasiveness of many cancer cells. In this study, the effects of propofol on hepatocellular carcinoma cells invasion ability were examined. METHODS: We assessed the invasion ability of HepG2 cells in vitro by determining enzyme activity and protein expression of MMP-9 using gelatin zymography assay and Western blot. The real-time PCR was used to evaluate the effect of propofol on microRNA-199a (miR-199a) expression, and miR-199a-2 precursor to evaluate whether over-expression of miR-199a can affect MMP-9 expression. Finally, the effect of miR-199a on propofol-induced anti-tumor activity using anti-miR-199a was assessed. RESULTS: Propofol significantly elevated the expression of miR-199a and inhibited the invasiveness of HepG2 cells. Propofol also efficiently decreased enzyme activity and protein expression of MMP-9. Moreover, the over-expression of miR-199a decreased MMP-9 protein level. Interestingly, the neutralization of miR-199a by anti-miR-199a antibody reversed the effect of propofol on alleviation of tumor invasiveness and inhibition of MMP-9 activity in HepG2 cells. CONCLUSION: Propofol decreases hepatocellular carcinoma cell invasiveness, which is partly due to the down-regulation of MMP-9 expression by miR-199a. | Jian Zhang Dan Zhang Guo-Qing Wu Zhi-Ying Feng Sheng-Mei Zhu | 2013 | Hepatobiliary & Pancreatic Diseases International2013，12，3： | 14 |
| 15 | Lymph node staging in colorectal cancer:Old controversies and recent advances显示文摘Outcome prediction based on tumor stage reflected by the American Joint Committee on Cancer(AJCC)/Union for International Cancer Control(UICC)tumor node metastasis(TNM)system is currently regarded as the strongest prognostic parameter for patients with colorectal cancer.For affected patients,the indication for adjuvant therapy is mainly guided by the presence of regional lymph node metastasis.In addition to the extent of surgical lymph node removal and the thoroughness of the pathologist in dissecting the resection specimen,several parameters that are related to the pathological work-up of the dissected nodes may affect the clinical significance of lymph node staging.These include changing definitions of lymph nodes,involved lymph nodes,and tumor deposits in different editions of the AJCC/UICC TNM system as well as the minimum number of nodes to be dissected.Methods to increase the lymph node yield in the fatty tissue include methylene blue injection and acetone compression.Outcome prediction based on the lymph node ratio,defined as the number of positive lymph nodes divided by the total number of retrieved nodes,may be superior to the absolute numbers of involved nodes.Extracapsular invasion has been identified as additional prognostic factor.Adding step sectioning and immunohistochemistry to the pathological work-up may result in higher accuracy of histological diagnosis.The clinical value of more recent technical advances,such as sentinel lymph node biopsy and molecular analysis of lymph nodes tissue still remains to be defined. | Annika Resch Cord Langner | 2013 | World Journal of Gastroenterology2013，19，46： | 14 |
| 16 | miR-132 inhibits colorectal cancer invasion and metastasis via directly targeting ZEB2显示文摘AIM:To investigate the biological role and underlying mechanism of miR-132 in colorectal cancer(CRC)progression and invasion.METHODS:Quantitative RT-PCR analysis was used to examine the expression levels of miR-132 in five CRC cell lines(SW480,SW620,HCT116,HT29 and LoVo)and a normal colonic cell line NCM460,as well as in tumor tissues with or without metastases.The KaplanMeier method was used to analyze the prognostic significance of miR-132 in CRC patients.The biological effects of miR-132 were assessed in CRC cell lines using the transwell assay.Quantitative RT-PCR and western blot analyses were employed to evaluate the expression of miR-132 targets.The regulation of ZEB2 by miR-132was confirmed using the luciferase activity assay.RESULTS:miR-132 was significantly down-regulated in the CRC cell lines compared with the normal colonic cell line(P<0.05),as well as in the CRC tissues withdistant metastases compared with the tissues without metastases(10.52±4.69 vs 23.11±7.84)(P<0.001).Down-regulation of miR-132 was associated with tumor size(P=0.016),distant metastasis(P=0.002),and TNM stage(P=0.020)in CRC patients.Kaplan-Meier survival curve analysis indicated that patients with low expression of miR-132 tended to have worse diseasefree survival than patients with high expression of miR-132(P<0.001).Moreover,ectopic expression of miR-132 markedly inhibited cell invasion(P<0.05)and the epithelial-mesenchymal transition(EMT)in CRC cell lines.Further investigation revealed ZEB2,an EMT regulator,was a downstream target of miR-132.CONCLUSION:Our study indicated that miR-132 plays an important role in the invasion and metastasis of CRC. | Yong-Bin Zheng Hai-Ping Luo Qiang Shi Zhi-Nan Hao Yu Ding Qiu-Shuang Wang Sheng-Bo Li Gao-Chun Xiao Shi-Lun Tong | 2014 | World Journal of Gastroenterology2014，20，21： | 14 |
| 17 | Impact of the red imported fire ant Solenopsis invicta Buren on biodiversity in South China: A review显示文摘The red imported fire ant, Solenopsis invicta, is a problematic invasive species in China since at least 2003. Over the past 15 years, a numerous studies were published on the impacts of this species on flora, fauna, and ecosystem function in natural and agricultural systems. We reviewed the literature on S. invicta invasion biology and impacts on biodiversity in South China. Both monogyne and polygyne colonies of S. invicta were introduced to China and polygyne colony is the dominant type. The range expansion rate of S. invicta may reach 26.5–48.1 km yr–1 in China. S. invicta forage activities occur year-round, peaking in the summer and fall in South China and show a preference for insects and plant seeds. We describe the ecological impacts of S. invicta on various habitats in South China, including arthropod community structure disruption and decreases in diversity and abundance of native ant species. S. invicta can replace the role of native ants in mutualisms between ants and honeydew-producing Hemiptera, which results in loss of important food resources for native ants and natural enemies of hemipterans. Further research is required to assess the complex ecosystem-level impacts of S. invicta in introduced areas. | WANG Lei XU Yi-juan ZENG Ling LU Yong-yue | 2019 | Journal of Integrative Agriculture2019，18，4： | 14 |
| 18 | Expression of MAPK1 in cervical cancer and effect of MAPK1 gene silencing on epithelial-mesenchymal transition,invasion and metastasis显示文摘Objective:To discuss the expression of mitogen-activated protein kinase 1(MAPK1) in the cervical cancer and effect of MAPK1 gene silencing on epithelial-mesenchymal transition and invasion and metastasis.Methods:Immunohistoehemistry,western blot and RT-PCR method were employed to detect the expression of MAPKl protein and mRNA in cervical cancer tissue and adjacent normal tissue.The constructed siRNA-MAPKI was transferred into human cervical cancer HeLa cells using Lipofectamine^(?)2000.MTT method was used to detect the cell vitality,transwell method to detect the cell invasion,and western blot to detect the expression of matrix metalloproteinases(MMP)-2,MMP-9,tissue inhibitor of metalloproteinase(TIMP)-1,TIMP-2,zinc finger transcription factor(Snail),epithelialmesenchymal transition related protein(EMT) E-cadherin and vimentin in cells.Results:The expression of MAPKl protein and mRNA in the cervical cancer tissue was significantly higher than the one in the adjacent normal tissue(P<0.01):after transfecting the siRNA-MAPKI into the human cervical cancer HeLa cells through liposome,compared with the control group,its cell vitality was significantly decreased(P<0.01),cell invasion was significantly decreased(P<0.01);expressed of MMP2.MMP-9,Snail and vimentin was significantly decreased(P<0.01),and expression of TIMP-1,TIMP-2 and E-cadherin was significantly increased(/J<0.01).Conclusions:Because of the high expression of MAPKl in the cervical cancer tissue,the interference in the expression of MAPK1 can significantly inhibit the invasion and metastasis of cervical cancer HeLa cells,which is related to the interference in the expression of MMPs/TIMP and Snail-mediated generation of EMT. | Xiao-Wen Li Muyasier Tuergan Guzhalinuer Abulizi | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，11： | 12 |
| 19 | Influence of up-regulation of Notch ligand DLL4 on biological behaviors of human gastric cancer cells显示文摘AIM: To investigate the potential roles of Delta-like ligand 4 (DLL4) on the biological behavior of gastric cancer cells and its molecular mechanisms. METHODS: A recombinant eukaryotic expression vector containing human DLL4 gene was constructed and transfected into the human gastric cancer cell line SGC7901. Clones with up-regulated DLL4 were selected and amplified. The effect of DLL4 up-regulation on gastric cancer cell growth was assessed using cell growth assay. The migration and invasion were assessed using a transwell migration assay and matrigel invasion assay. Matrix metalloproteinases were detected using the zymogram technique. Cells were implanted subcutaneously into male BALB/c nu/nu mice. Tumor volumes were then calculated and compared. DLL4 staining in the implanted tumor was performed using immunohistochemistry technique. RESULTS: Growth curves over a six-day time course showed significantly promoted cell proliferation of SGC7901 cells with up-regulated DLL4. DLL4 up-regulation in SGC7901 cells promoted the migration (205.4 ± 15.2 vs 22.3 ± 12.1, P < 0.05) and invasion (68.8 ± 5.3 vs 18.2 ± 6.0, P < 0.05) in vitro and tumorigenicity in vivo (2640.5 ± 923.6 mm 3 vs 1115.1 ± 223.8 mm 3 , P < 0.05). Furthermore, significantly increased mRNA level and increased secretion of matrix metalloproteinase-2 (MMP-2) proenzyme were observed in SGC7901 cells with up-regulated DLL4. However, increased MMP-9 mRNA level but decreased extracellular MMP-9 proenzyme level was observed. CONCLUSION: Our observations indicated a mechanism by which activation of DLL4-mediated Notch signaling promotes the expression and secretion of MMP-2 proenzyme and influences the progress of gastric cancer. | Guo-Gang Li Lan Li Chao Li Long-Yun Ye Xiao-Wen Li Da-Ren Liu Qi Bao Yi-Xiong Zheng Da-Peng Xiang Li Chen Jian Chen | 2013 | World Journal of Gastroenterology2013，19，28： | 12 |
| 20 | MiR-122-5p suppresses the proliferation, migration, and invasion of gastric cancer cells by targeting LYN显示文摘Gastric cancer(GC)is one of malignant tumors with high mortality and morbidity in the world.MicroRNA-122(miR-122)acts as a tumor suppressor in a variety of cancers and has been found to be dominant in gastric adenocarcinoma.However,the specific biological function of miR-122-5p in GC is not completely clear.In this study,we found that miR-122-5p was low-expressed in GC tissues and cell lines by using qRT-PCR.Overexpression of miR-122-5p inhibited the proliferation,migration,and invasion of GC cells by using CCK-8 and transwell assays.On the contrary,downregulation of miR-122-5p promoted the proliferation,migration,and invasion of GC cells.In addition,we found that the expression of LYN,an Src family tyrosine kinase,was inversely correlated with miR-122-5p expression in GC tissues by using western blot analysis,immunohistochemistry,and qRT-PCR assays.Meanwhile,luciferase assay results indicated that LYN is a direct target of miR-122-5p in GC cells.Moreover,silencing LYN expression by its siRNA inhibited the proliferation,migration,and invasion of GC cells.Importantly,overexpression of LYN restored miR-122-5p-mediated inhibition of the proliferation,migration,and invasion of GC cells.Taken together,our results indicated miR-122-5p inhibited the proliferation,migration,and invasion by targeting LYN in GC. | Lei Meng Zhangming Chen Zhe Jiang Ting Huang Jie Hu Panquan Luo Hongli Zhang Mengqi Huang Lei Huang Yu Chen Ming Lu A-man Xu Songcheng Ying | 2020 | Acta Biochimica et Biophysica Sinica2020，52，1： | 12 |
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