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| 1 | Apoptosis,proliferation and p53 gene expression of H.pylori associated gastric epithelial lesions显示文摘AIM: To study the relationship between Helicobacter pylori (H. Pylori) and gastric carcinoma and its possible pathogenesis by H. Pylori.METHODS: DNEL technique and immunohistochemical technique were used to study the state of apoptosis,proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30H. Pylori-negative and 30 H. Pylorf-positive gastric precancerous lesions along with 20 gastric carcinomas were studied.RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (Al, 4.36% ± 1.95%), proliferative index (PI, 19.11% ± 6.79%) and positivity of p53 expression (46.7%) in H. Pylori-positive group were higher than those in normal mucosa (P< 0.01). Al in H. Pylori-positive group was higher than that in H. Pylori-negative group (3.81% ±1.76%), PI in H. Pylori-positive group was higher than that in H. Pylori-negative group (12.25% ±5.63%, P<0.01 ). In the phase of dysplasia, Al (2.31% ± 1.10%) in H. Pylori-positive group was lower (3.05% ± 1.29%) than that in H. Pylori-negative group, but PI (33.89% ± 11.65%)wassignificantly higher(22.09± 8018%, P< 0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. Pylori-positive group, Als had an evidently graduall decreasing trend (P < 0.01 ), while Pis had an evidently gradual increasing trend (P< 0.05 or P< 0.01), and there was also a trend of gradual increase in the expression of p53 gene.CONCLUSION: In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. Pylori, and H. Pylori can induce apoptosis in the phase of metaplasia but in the phase of dysplasia H.pylori can inhibit cellular apoptosis. And H. Pylori infection can strengthen the expression of mutated p53 gene. | Zhong Zhang~1 Yuan Yuan Hua Gao Ming Dong Lan Wang Yue-Hua Gong 1 Department of Pathology,Shenyang Medical College,Shenyang 110031 Liaoning Province,China | 2001 | World Journal of Gastroenterology2001，7，6： | 46 |
| 2 | CCK-8法与MTT法检测人前列腺癌PC3细胞活性的比较研究显示文摘目的探讨CCK-8法和MTT法的最佳实验条件。方法以人前列腺癌PC3细胞作为研究对象,采用CCK-8和MTT法检测抗肿瘤药物阿霉素(ADM)对PC3细胞增殖的影响。结果 CCK-8法的最佳检测波长为450 nm,最佳检测时间为加入CCK-8试剂后4 h,适宜细胞数量范围为8×102~1×105个。结论 CCK-8法较MTT法检测的灵敏度高,准确性好,是一种优于MTT法的检测细胞增殖活性的方法。 | 万文婷 李宁 刘静 金林红 | 2010 | 时珍国医国药2010，21，12： | 31 |
| 3 | FoxO3a and disease progression显示文摘The Forkhead box O(FoxO) family has recently been highlighted as an important transcriptional regulator of crucial proteins associated with the many diverse functions of cells. So far, FoxO1, FoxO3 a, FoxO4 and FoxO6 proteins have been identified in humans. Although each FoxO family member has its own role, unlike the other FoxO families, FoxO3 a has been extensively studied because of its rather unique and pivotal regulation of cell proliferation, apoptosis, metabolism, stress management and longevity. FoxO3 a alteration is closely linked to the progression of several types of cancers, fibrosis and other types of diseases. In this review, we will examine the function of FoxO3 a in disease progression and also explore FoxO3a's regulatory mechanisms. We will also discuss FoxO3 a as a potential target for the treatment of several types of disease. | Richard Seonghun Nho Polla Hergert | 2014 | World Journal of Biological Chemistry2014，5，3： | 28 |
| 4 | Inhibitory effect of norcantharidin on the growth of human gallbladder carcinoma GBC-SD cells in vitro显示文摘 | Fan, Yue-Zu Fu, Jin-Ye Zhao, Ze-Ming Chen, Chun-Qiu | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，1： | 25 |
| 5 | Effects of salvianolic acid-A on NIH/3T3 fibroblast proliferation,collagen synthesis and gene expression显示文摘AIM To investigate the mechanisms ofsalvianolic acid A(SA-A)against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10-4mol/L-10-7mol/L SA-A for 22 h.The cell viability wasassayed by[3H]proline incorporation,cellproliferation by[3H]TdR incorporation,cellcollagen synthetic rate was measured with[3H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α(1)I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10-4mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10-5mol/L-10-7mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10-6mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10-5mol/L-10-6mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10-5mol/L and10-6mol/L SA-A could decrease α(1)I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug. | Liu CH Hu YY Wang XL Liu P Xu LM | 2000 | World Journal of Gastroenterology2000，6，3： | 25 |
| 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 | The Property of Solution of a Nonstationary Forest Evolution System | WANG Dingjiang Department of Mathematics, Pingdingshan Teacher’s College, He’nan 467000ZHANG Yufeng Department of Mathematics, Yanbian Teacher’s College, Jilin 133000 | 1993 | Systems Science and Systems Engineering1993，3，3： | 23 |
| 8 | The altered PD-1/PD-L1 pathway delivers the ‘one-two punch’ effects to promote the Treg/Th17 imbalance in pre-eclampsia显示文摘The programmed cell death-1(PD-1)/PD-ligand 1(PD-L1)pathway is critical for normal pregnancy by promoting regulatory T(Treg)cell development and inhibiting the Th17 response.However,the relationship between the PD-1/PD-L1 pathway and the Treg/Th17 imbalance in pre-eclampsia(PE)is an enigma.In this study,decreased PD-1 and PD-L1 expression and a Treg/Th17 imbalance were observed at the maternal-fetal interface in PE.The regulatory effects of the PD-1/PD-L1 pathway on the Treg and Th17 cell quantities were determined in vitro by targeting T-cell proliferation,differentiation and transdifferentiation.First,decreased PD-1 expression might contribute to a higher Th17 cell frequency by promoting proliferation in PE.Second,the percentages of Treg but not Th17 cells differentiated from peripheral naive CD4+T cells were increased by PD-L1 Fc administration.This effect was accompanied by decreased PI3K/AKT/m-TOR and increased PTEN mRNA expression and was completely reversed by PD-1 blockade.Finally,the percentage of IL-17-producing Treg cells increased and was positively associated with the Th17 cell frequency in PE.Increased RORγt and IL-17 but not Foxp3 and IL-10 mRNA expression by Treg cells was observed with PD-1 blockade.Similar findings occurred when Treg cells were exposed to IL-6/IL-23/IL-1βand were reversed by PD-L1 Fc.Taken together,our findings indicate that the PD-1/PD-L1 pathway contributes to the Treg/Th17 imbalance via‘one-two punch’approaches:(i)promoting Th17 cell proliferation,(ii)inhibiting Treg cell differentiation and(iii)enhancing Treg cell plasticity into Th17 cells in PE.The therapeutic value of PD-L1 Fc for PE treatment will be explored in the future. | Yonghong Zhang Zhaozhao Liu Mei Tian Xiaohui Hu Liling Wang Jinlu Ji Aihua Liao | 2018 | Cellular & Molecular Immunology2018，15，7： | 21 |
| 9 | Effects of salvianolic acid B on proliferation, neurite outgrowth and differentiation of neural stem cells derived from the cerebral cortex of embryonic mice显示文摘Salvianolic acid B is isolated from Salvia miltiorrhiza,the root of which is widely used as a traditional Chinese medicine to treat stroke.However,little is known about how salvianolic acid B influences growth characteristics of neural stem cells (NSCs).The purpose of the present study was to evaluate the effects of salvianolic acid B on proliferation,neurite outgrowth and differentiation of NSCs derived from the cerebral cortex of embryonic mice using MTT,flow cytometry,immunofluorescence and RT-PCR.It was found that 20 μg mL·1 and 40 μg mL·1 salvianolic acid B had similar effects on proliferation of NSCs,and a suitable concentration of salvianolic acid B increased the number of NSCs and their derivative neurospheres.The growth-promoting activity of salvianolic acid B was dependent on and associated with an accumulation in the G2/S-phase cell population.Salvianolic acid B also promoted the neurite outgrowth of NSCs and their differentiation into neurons.The mRNA for tau,GFAP and nestin were present in differentiating neurospheres induced by salvianolic acid B.However,high-level expression of tau mRNA and low-level expression of GFAP mRNA was detected in differentiated cells,in contrast to the control conditions.This collective evidence indicates that exogenous salvianolic acid B is capable of promoting proliferation of neurospheres and differentiation towards the neuronal lineage in vitro and may act in the proliferation of NSCs and may promote NSC differentiation into neuronal cells. | GUO GuoQing1,LI Bin1,WANG YuanYuan1,SHAN AiJing1,SHEN WeiZai1,YUAN Lin2 & ZHONG ShiZhen2 1Department of Anatomy,Medical College of Jinan University,Guangzhou 510630,China 2Institute of Clinical Anatomy,Key Laboratory of Tissue Construction and Detection of Guangdong Province,Southern Medical University,Guangzhou 510150,China | 2010 | Science China(Life Sciences)2010，53，6： | 21 |
| 10 | Inhibition of 12-lipoxygenase reduces proliferation and induces apoptosis of hepatocellular carcinoma cells in vitro and in vivo显示文摘BACKGROUND:12-lipoxygenase(12-LOX) has been reported to be an important gene in cancer cell proliferation and survival,and tumor metastasis.However,its role in hepatocellular carcinoma(HCC) cells remains unknown.METHODS:Expression of 12-LOX was assessed in a diethylnitrosamine-induced rat HCC model,and in SMMC-7721,HepG2 and L-02 cells using immunohistochemical staining and reverse transcriptase-polymerase chain reaction(RT-PCR).GST-π and Ki-67 were determined in vivo by immunohistochemical staining.Apoptosis was evaluated by TUNEL assay.Cell viability and apoptosis were determined by MTT assay and flow cytometry,respectively.Apoptosis-related proteins in SMMC-7721 and HepG2 cells were detected by Western blotting.RESULTS:Immunohistochemical staining and RT-PCR showed that 12-LOX was over-expressed in rat HCC and two HCC cell lines,while the expression was inhibited by baicalein,a specific inhibitor of 12-LOX.Baicalein inhibited cell proliferation and induced apoptosis in rat HCC and both cell lines in a dose-and time-dependent manner.Our in vivo study demonstrated that baicalein also reduced neoplastic nodules.Mechanistically,baicalein reduced Bcl-2 protein expression coupled with a slight increase of the expression of Bax and activation of caspase-3.Furthermore,baicalein inhibited the activation of ERK-1/2(phosphorylated).Interestingly,the effects of baicalein were reversed by 12(S)-HETE,a metabolite of 12-LOX.CONCLUSIONS:Inhibition of 12-LOX leads to reduced numbers of HCC cells,partially caused by increased apoptosis.12-LOX may be a potential molecular target for HCC prevention and treatment. | Xi-Ming Xu,Guang-Jin Yuan,Jun-Jian Deng,Hong-Ting Guo,Miao Xiang,Fang Yang,Wei Ge and Shi-You Chen Cancer Center, Renmin Hospital of Wuhan University, Wuhan 430060, China Cancer Center, the 82nd Hospital of the Chinese PLA, Huai’an 223001, China Department of Physiology, Medical College of Wuhan University, Wuhan 430071, China Department of Physiology & Pharmacology, University of Georgia, Athens, GA 30602, USA | 2012 | Hepatobiliary & Pancreatic Diseases International2012，11，2： | 20 |
| 11 | microRNA-181b targets MLK2 in HL-60 cells显示文摘microRNAs(miRNAs) play critical roles in many different cellular processes,including metabolism,apoptosis,differentiation and development.We showed miR-181b to be highly expressed in acute myeloid leukemia(AML).Furthermore,miR-181b contributed to proliferation of AML cells by targeting MLK2.Our results demonstrated that miR-181b plays an important role in the biology of AML and may be useful in developing therapies targeting miRNAs. | CHEN Hong1,CHEN Qun2,FANG Ming3 & MI Yan1 1 The First Affiliated Hospital of Harbin Medical University,Harbin 150101,China 2 Harbin Acheng District People’s Hospital,Harbin 150300,China 3 Graduate Department of Harbin Medical University,Harbin 150001,China | 2010 | Science China(Life Sciences)2010，53，1： | 20 |
| 12 | 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 |
| 13 | Effects of ginsenoside Rh2 on growth and migration of pancreatic cancer cells显示文摘AIM:To investigate the effects of ginsenoside Rh2 on the human pancreatic cancer cell line Bxpc-3.METHODS:The human pancreatic cancer cell line Bxpc-3 was cultured in vitro and treated with or without ginsenoside Rh2.Growth rates for Bxpc-3 cells were assessed by methyl thiazolyl tetrazolium(MTT) and colony formation assays.Cell cycle changes were analyzed by flow cytometry.Apoptosis was measured by flow cytometry and Hoechst 33258 fluorescence staining.A scratch assay and a Matrigel invasion assay were used to detect cell migration and invasion.Expression of Bax,Bcl-2,survivin,cyclin D1,matrix metalloproteinase(MMP)-2,MMP-9,cleaved caspase-3,caspase-8,and caspase-9 mRNA were determined by reverse transcriptase-polymerase chain reaction(RT-PCR).Bax,Bcl-2,survivin,cyclin D1,cleaved caspase-3,caspase-8 and caspase-9 protein levels were examined by western blotting.Expression of MMP-2 and MMP-9 proteins in culture supernatants were determined by enzymelinked immunosorbent assay(ELISA).RESULTS:Rh2 significantly inhibited Bxpc-3 cell proliferation in a dose-and time-dependent manner,as evaluated by the MTT(P < 0.05) and colony formation assays(P < 0.05).Compared to the control group,Rh2 significantly increased the percentage of Bxpc-3 cells in the G 0 /G 1 phase from 43.32% ± 2.17% to 71.32% ± 1.16%,which was accompanied by a decrease in S phase(from 50.86% ± 1.29% to 28.48% ± 1.18%) and G 2 /M phase(from 5.81% ± 1.19% to 0.20% ± 0.05%) in a dose-dependent manner(P < 0.05),suggesting that Rh2 arrested cell cycle progression at the G 0 /G 1 phase,as measured by flow cytometry.Compared to the control group,cells treated with Rh2 showed significantly higher apoptosis ratios in a dosedependent manner(percentage of early apoptotic cells:from 5.29% ± 2.28% to 38.90% ± 3.42%(F = 56.20,P < 0.05);percentage of late apoptotic cells:from 4.58% ± 1.42% to 36.32% ± 2.73%(F = 86.70,P < 0.05).Rh2 inhibited Bxpc-3 cell migration and invasion,as detected by scratch wound healing assay and Matrigel invasion assay [percentages of scratch wound healing for 12 h,24 h and 48 h(control vs experimental group):37.3% ± 4.8%vs 18.30% ± 1.65%,58.7% ± 3.5% vs 38.00% ± 4.09% and 93.83% ± 4.65% vs 65.50% ± 4.09%,respectively;t = 6.489,t = 6.656 and t = 7.926,respectively,P < 0.05;the number of cells invading at various concentrations(0 μmol/L,35 μmol/L,45 μmol/L and 55 μmol/L):81.10 ± 9.55,46.40 ± 6.95,24.70 ± 6.88 and 8.70 ± 3.34,respectively(F = 502.713,P < 0.05)].RT-PCR,western blotting or ELISA showed that mRNA and protein expression of Bax,cleaved caspase-3 and caspase-9 were upregulated(P < 0.05),while mRNA and protein expression of Bcl-2,survivin,cyclin D1,MMP-2 and MMP-9 were downregulated(P < 0.05).CONCLUSION:Ginsenoside Rh2 inhibits proliferation,migration and invasion and induces apoptosis of the human pancreatic cancer cell line Bxpc-3. | Xi-Ping Tang Guo-Du Tang Chun-Yun Fang Zhi-Hai Liang Lu-Yi Zhang | 2013 | World Journal of Gastroenterology2013，19，10： | 19 |
| 14 | Effect of lipid on proliferation and activation of rat hepatic stellate cells(Ⅰ)显示文摘INTRODUCTIONDespitetheearlycontroversyovertheprimarycelularsourceofextracelularmatrixproteinsinliverfibrosis,compelinginvitro... | LU Lun Gen, ZENG Min De, LI Ji Qiang, HUA Jing, FAN Jian Gao, FAN Zhu Ping and QIU De Kai | 1998 | World Journal of Gastroenterology1998，4，6： | 18 |
| 15 | The proliferation, differentiation, and mineralization effects of puerarin on osteoblasts in vitro显示文摘AIM: Osteoblasts are key functional cells in the process of bone metabolic balance. Phytoestrogens have an important influence on the proliferation and differentiation of osteoblasts. Puerarin, a plant estrogen, has a wide range concentration in vitro on the function of osteoblasts. The current study investigates the effect of the phytoestrogen puerarin on the proliferation, differentiation, and mineralization of osteoblasts in vitro. METHODS: The calvaria bone of eight-ten Wistar rats which were born within 24 h were obtained in aseptic condition. After enzyme digestion, isolation, purified osteoblasts of rats were cultured for further study. The cells of the first to third generation were divided into a control group and a puerarin-treated group with 10-3–10-10 mol·L-1 puerarin. The cells were exposed to the medium containing a low level of carbohydrates, 10%(V/V) FBS for 24 h. After 1 to 4 days of culture, the OD values on the proliferation of osteoblasts in each group were determined by microplate reader. The cells were cultured in the medium containing 50 μg·mL-1 vitamin C, 10-2 mol·L-1 sodium glycerophosphate, 10% FBS and the medium was changed every 3 to 4 days. After 2 to 8 days of culture, expression of alkaline phosphatase were tested and compared by microplate reader. The mineral nodes of osteoblasts were dyed using alizarin red or improved Von Kossa way after four weeks. RESULTS: Compared with those in the 10-5–10-9 mol·L-1 puerarin, the proliferation of osteoblasts, the expression of alkaline phosphatase, and the number of mineral nodes of osteoblasts were significantly decreased in the control group. The increase was the fastest in the third day, while on the fourth day it was decreased, and arrived at statistical significance compared with the alkaline phosphatase activities and control group. The 10-6 mol·L-1 group was the most distinct, and formed the most mineralized nodule. Compared with the 10-3 mol·L-1 puerarin group, those changes were markedly increased in the control group. CONCLUSIONS: Puerarin has proliferation, differentiation, and mineralization effects on osteoblasts in a dose-dependent manner, and has a double-way effect on the osteoblasts in vitro. A low-dose showed positive effects on the development of osteoblasts, and high-dose puerarin could inhibit the formation of bone. | WANG Chang MENG Mei-Xia TANG Xu-Lei CHEN Ke-Ming ZHANG Li LIU Wei-Ning ZHAO Ying-Yong | 2014 | Chinese Journal of Natural Medicines2014，12，6： | 18 |
| 16 | Hepatitis B virus X protein promotes proliferation and upregulates TGF-β1 and CTGF in human hepatic stellate cell line,LX-2显示文摘BACKGROUND:Chronic hepatitis B virus(HBV)infection is a major cause of liver fibrosis,but the mechanisms underlying HBV-related fibrogenesis are still unknown. Although the roles of HBV X protein(HBx)remain poorly understood,it is thought to play an important role in the regulation of cellular growth and hepatocarcinogenesis. The aim of this study was to determine the role of HBx in liver fibrogenesis by studying the effect of HBx on the proliferation and expression of fibrosis-related molecules in the human hepatic stellate cell line,LX-2. METHODS:We established an in vitro co-culture system with LX-2 cells and a stable QSG7701-HBx cell line which had been transfected with the HBx gene. 3 H-TdR incorporation and flow cytometry were used to determine the effects of HBx on the proliferation of LX-2 cells. α-smooth muscle actin(α-SMA),transforming growth factor-β1(TGF-β1),transforming growth factor-βreceptor Ⅱ(TGF-βRⅡ),and connective tissue growth factor (CTGF)in LX-2 cells were analyzed by Western blotting.In addition,the expression levels of collagen typeⅠ(ColⅠ) from the co-cultured media were measured by ELISA. RESULTS: 3 H-TdR incorporation increased significantly in LX-2 cells co-cultured with QSG7701-HBx cells compared to those cultured with QSG7701-pcDNA3 and QSG7701 (non-tumorigenic human liver cell line).Cell cycle results revealed that HBx accelerated the progression of G1 to S in LX-2 cells.The expressions ofα-SMA,TGF-β1,TGF-βRⅡ,CTGF and ColⅠwere significantly increased in the co- cultures of LX-2 cells with stable QSG7701-HBx cells. CONCLUSION:These results suggest that HBx may facilitate liver fibrosis by promoting hepatic stellate cell proliferation and upregulating the expression of fibrosis- related molecules. | Guang-Hui Guo,De-Ming Tan,Ping-An Zhu and Fei Liu Department of Infectious Diseases,Xiangya Hospital,Central South University,Changsha 410008,China | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，1： | 17 |
| 17 | Effect and molecular mechanism of mir-146a on proliferation of lung cancer cells by targeting and regulating MIF gene显示文摘Objective: To discuss the effect and molecular mechanism of mi R-146 a on the proliferation of lung cancer cells by targeting and regulating the macrophage migration inhibitory factor(MIF) gene. Methods: RT-PCR was employed to detect expression of mi R-146a; immunohistochemistry was used to detect the expression of MIF. The luciferase reporter gene technique was adopted to verify that MIF was the specific reverse target gene of mi R-146 a and the liposome LipofectamineTM2000 was employed to transfer the modeled mi R-146 a mimics, and mi R-146 a negative control(NC) in NSCLC cells to detect the expression of MIF m RNA and protein. MTT assay was used to detect cell viability, cloning technique to detect cell proliferation ability, Annexin V-PI to detect cell apoptosis, UV spectrophotometry to detect viability of cysteinyl aspartate specific proteinase 3(Caspase 3), and western blot to detect expression of nuclear factor-κB(NF-κB) in cells. Results: The expression of mi R-146 a in NSCLC lung tissues was lower than that in the normal lung tissues besides the lung cancer; while the expression of mi R-146 a in NSCLC cells was lower than that in normal human embryonic lung tissues. It was chosen as the subsequent cell line for its appropriate expression in A549. The expression of MIF protein in NSCLC lung tissues was higher than that in the normal lung tissues besides the lung cancer. The luciferase reporter gene proved that MIF was the reverse target gene of mi R-146 a. The mi R-146 a mimics were transfected into A549 cells through the liposome. Compared with NC group, the expression of MIF protein and m RNA was significantly decreased(P<0.01), with the decrease in the cell viability(P<0.01), the decrease in the number of clones(P<0.01), cell apoptosis(P<0.01), the increase in the activity of Caspase 3(P<0.01), and decrease in the phosphorylation of NF-κB p65(P<0.01). Conclusions: mi R-146 a has low expression in NSCLC tissues and cell lines, while MIF has the over expression in NSCLC tissues. The increased expression of mi R-146 a can inhibit the expression of MIF via the gene targeting and thus inhibit the proliferation of A549 cells and induce the apoptosis of cancer cells, which may be realized through NF-κB signaling pathway. | Wu-Ming Wang Ji-Chun Liu | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，8： | 17 |
| 18 | Inhibitory effects of Curcuma aromatica oil on proliferation of hepatoma in mice显示文摘AIM To reveal the inhibitory effects ofCurcuma aromatica oil(CAO)on cellproliferation of hepatoma in mice.METHODS Two tumor inhibitory experimentsof CAO on hepatoma in mice were conducted.The inhibitory effects of CAO on proliferation ofhepatoma in mice were evaluated by DNA imagecytometry and immunohistochemical staining ofproliferating cell nuclear antigen(PCNA).RESULTS The tumor inhibitory rates of CAOwere 52% and 51% in two experiments,respectively.Compared with those of the saline-treated control groups,both differences werestatistically significant(P<0.01).In the groupof mice treated with CAO,the cellular nuclearDNA OD value(249±70),areas(623 μm^2±228 μm^2)and DNA(2.38±0.67)index of hepaticcarcinomas were significantly lower than thoseof the control group(430±160,1073 μm^2±101 μm^2 and 4.48±0.71).CAO also couldincrease diploidy cell rates(29.00%±9.34% vs2.97%±5.69%,P<0.01)and decreasepentaploidy cell exceeding rate(30.04%±15.10% vs 70.89%±14.94%,P<0.01).In thegroup of mice treated with CAO,the labelingindexes of proliferating cell nuclear antigen (PCNA-LI)were 30%±4%,which weresignificantly lower than 40%±6% of the controlgroup(P<0.01).CONCLUSION The inhibition of CAO on thegrowth of hepatoma in mice might be associatedwith its depression on cellular proliferativeactivity. | Wan Yin Wu Qin Xu Ling Chun Shi Wei Bin Zhang | 2000 | World Journal of Gastroenterology2000，6，2： | 16 |
| 19 | 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 |
| 20 | miR-129-5p suppresses proliferation, migration, and induces apoptosis in pancreatic cancer cells by targeting PBX3显示文摘Pancreatic cancer(PC)is the seventh m ost frequent cause of cancer-related deaths world wide with a high mortality.MicroRNAs(miRNAs)act as im portant regulators for the developm ent of PC and participate in the progression of PC.miR-129-5p was reported to regulate the progression of tum ors,such as thyroid cancer and gastric cancer.However,the function of miR-129-5p in PC is still unclear.In this study,the down-regulation of miR-129-5p was detected in PC tissues and PC cells.miR-129-5p was overexpressed or knocked down in AsPC-1 and BxPC-3 cells.The results showed that miR-129-5p overexpression suppressed proliferation,m igration and invasion,and induced apoptosis of PC cells,whereas miR-129-5p knockdown showed opposite effects:In addition,we found that pre-B-cell leukemia hom eobox 3(PBX3)overexpression prom oted proliferation,m igration and invasion,but reduced apoptosis of PC cells.PBX3 was identified as a target of miR-129-5p by inform atics analysis and dual luciferase reporter assay.Finally,our results indicated that miR-129-5p suppressed cell proliferation and m igration by targeting PBX3.This study dem onstrated that miR-129-5p could function as a tu m o r suppressor in the progression and developm ent of PC by targeting PBX3,providing a reliable prognostic factor and a new therapeutic strategy for PC. | Zhisheng Qiu Xiaochun Wang Yuping Shi Mingxu Da | 2019 | Acta Biochimica et Biophysica Sinica2019，51，10： | 15 |
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