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| 1 | Crustal structure of northeastern margin of the Tibetan Plateau by receiver function inversion显示文摘Using seismic data of about one year recorded by 18 broadband stations of ASCENT project,we obtained 2547 receiver functions in the northeastern Tibetan Plateau.The Moho depths under 14 stations were calculated by applying the H-κ domain search algorithm.The Moho depths under the stations with lower signal-noise ratio(SNR) were estimated by the time delay of the PS conversion.Results show that the Moho depth varies in a range of ~40–60 km.The Moho near the Haiyuan fault is vague,and its depth is larger than those on its two sides.In the Qinling-Qilian Block,the Moho becomes shallower gradually from west to east.To the east of 105°E,the average depth of the Moho is 45 km,whereas the west is 50 km or even deeper.Combining our results with surface wave research,we suggest a boundary between the Qinling and the Qilian Mountains at around 105°E.S wave velocities beneath 15 stations have been obtained through a linear inversion by using Crust2.0 as an initial model,and the crustal thickness that was derived by H-κ domain search algorithm was also taken into account.The results are very similar to the results of previous active source studies.The resulting figure indicates that low velocity layers developed in the middle and lower crust beneath the transition zone of the Tibet Block and western Qinling,which may be related to regional faults and deep earth dynamics.The velocity of the middle and lower crust increases from the Songpan Block to the northeastern margin of Tibetan Plateau.Based on the velocity of the crust,the distribution of the low velocity zone and the composition of the curst(Poisson's ratio),we infer that the crust thickening results from the crust shortening along the direction of compression. | LIU QiMin ZHAO JunMeng LU Fang LIU HongBing | 2014 | Science China Earth Sciences2014，57，4： | 23 |
| 2 | Whole-genome sequencing of 508 patients identifies key molecular features associated with poor prognosis in esophageal squamous cell carcinoma显示文摘Esophageal squamous cell carcinoma(ESCC)is a poor-prognosis cancer type with limited understanding of its molecular etiology.Using 508 ESCC genomes,we identified five novel significantly mutated genes and uncovered mutational signature clusters associated with metastasis and patients’outcomes.Several functional assays implicated that NFE2L2 may act as a tumor suppressor in ESCC and that mutations in NFE2L2 probably impaired its tumor-suppressive function,or even conferred oncogenic activities.Additionally,we found that the NFE2L2 mutations were significantly associated with worse prognosis of ESCC.We also identified potential noncoding driver mutations including hotspot mutations in the promoter region of SLC35E2 that were correlated with worse survival.Approximately 5.9%and 15.2%of patients had high tumor mutation burden or actionable mutations,respectively,and may benefit from immunotherapy or targeted therapies.We found clinically relevant coding and noncoding genomic alterations and revealed three major subtypes that robustly predicted patients’outcomes.Collectively,we report the largest dataset of genomic profiling of ESCC useful for developing ESCC-specific biomarkers for diagnosis and treatment. | Yongping Cui Hongyan Chen Ruibin Xi Heyang Cui Yahui Zhao Enwei Xu Ting Yan Xiaomei Lu Furong Huang Pengzhou Kong Yang Li Xiaolin Zhu Jiawei Wang Wenjie Zhu Jie Wang Yanchun Ma Yong Zhou Shiping Guo Ling Zhang Yiqian Liu Bin Wang Yanfeng Xi Ruifang Sun Xiao Yu Yuanfang Zhai Fang Wang Jian Yang Bin Yang Caixia Cheng Jing Liu Bin Song Hongyi Li Yi Wang Yingchun Zhang Xiaolong Cheng Qimin Zhan Yanhong Li Zhihua Liu-Show | 2020 | Cell Research2020，30，10： | 19 |
| 3 | miR-503-3p promotes epithelialemesenchymal transition in breast cancer by directly targeting SMAD2 and E-cadherin显示文摘Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of mi R-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined.Here, we found that mi R-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified mi R-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of mi R-503-3p in breast cancer cells inhibited expression of epithelialemesenchymal transition(EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their m RNA30 untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for mi R-503-3p in induction of breast cancer EMT and suggest that plasma mi R-503-3p may be a useful diagnostic biomarker for breast cancer. | Zitong Zhao Xinyi Fan Lanfang Jiang Zhongqiu Xu Liyan Xue Qimin Zhan Yongmei Song | 2017 | Journal of Genetics and Genomics2017，44，2： | 15 |
| 4 | A Multiscale Understanding of the Thermodynamic and Kinetic Mechanisms of Laser Additive Manufacturing显示文摘 | Dongdong Gu Chenglong Ma Mujian Xia Donghua Dai Qimin Shi | 2017 | Engineering2017，3，5： | 15 |
| 5 | Selective laser melting 3D printing of Ni-based superalloy: understanding thermodynamic mechanisms显示文摘A mesoscopic model has been established to investigate the thermodynamic mechanisms and densification behavior of nickel-based superalloy during additive manufacturing/three-dimensional(3D) printing(AM/3DP)by numerical simulation, using a finite volume method(FVM). The influence of the applied linear energy density(LED) on dimensions of the molten pool, thermodynamic mechanisms within the pool, bubbles migration and resultant densification behavior of AM/3DP-processed superalloy has been discussed. It reveals that the center of the molten pool slightly shifts with a lagging of 4 lm towards the center of the moving laser beam. The Marangoni convection, which has various flow patterns, plays a crucial role in intensifying the convective heat and mass transfer, which is responsible for the bubbles migration and densification behavior of AM/3DP-processed parts. At an optimized LED of 221.5 J/m, the outward convection favors the numerous bubbles to escape from the molten pool easily and the resultant considerably high relative density of 98.9 % is achieved. However, as the applied LED further increases over 249.5 J/m, the convection pattern is apparently intensified with the formation of vortexes and the bubbles tend to be entrapped by the rotating flow within the molten pool, resulting in a large amount of residual porosity and a sharp reduction in densification of the superalloy. The change rules of the relative density and the corresponding distribution of porosity obtained by experiments are in accordance with the simulation results. | Mujian Xia Dongdong Gu Guanqun Yu Donghua Dai Hongyu Chen Qimin Shi | 2016 | Science Bulletin2016，61，13： | 13 |
| 6 | Design and Optimization of Wheel-legged Robot:Rolling-Wolf显示文摘Though the studies of wheel-legged robots have achieved great success, the existing ones still have defects in load distribution, structure stability and carrying capacity. For overcoming these shortcomings, a new kind of wheel-legged robot(Rolling-Wolf) is designed. It is actuated by means of ball screws and sliders, and each leg forms two stable triangle structures at any moment, which is simple but has high structure stability. The positional posture model and statics model are built and used to analyze the kinematic and mechanical properties of Rolling-Wolf. Based on these two models, important indexes for evaluating its motion performance are analyzed. According to the models and indexes, all of the structure parameters which influence the motion performance of Rolling-Wolf are optimized by the method of Archive-based Micro Genetic Algorithm(AMGA) by using Isight and Matlab software. Compared to the initial values, the maximum rotation angle of the thigh is improved by 4.17%, the maximum lifting height of the wheel is improved by 65.53%, and the maximum driving forces of the thigh and calf are decreased by 25.5% and 12.58%, respectively. The conspicuous optimization results indicate that Rolling-Wolf is much more excellent. The novel wheel-leg structure of Rolling-Wolf is efficient in promoting the load distribution, structure stability and carrying capacity of wheel-legged robot and the proposed optimization method provides a new approach for structure optimization. | LUO Yang LI Qimin LIU Zhangxing | 2014 | Chinese Journal of Mechanical Engineering2014，27，6： | 12 |
| 7 | Enhanced Expression of miR-425 Promotes Esophageal Squamous Cell Carcinoma Tumorigenesis by Targeting SMAD2显示文摘Esophageal squamous cell carcinoma(ESCC) is one of the most common and deadly cancers in the world. Currently, clinical therapy of ESCC remains limited and the five-year survival rate is poor. The function of miR-425 has been reported in multiple human cancers.However, the tumorigenic role and clinical significance of miR-425 in ESCC remains unclear. We found that enhanced expression of miR-425 in ESCC cell lines not only promoted cell proliferation and colony formation, but also increased cellular metastasis. Furthermore, we revealed the mechanism that miR-425 inhibited the expression of SMAD2 by targeting the second binding site in the 30-untranslated region(30-UTR) in ESCC. This mode of action influenced not only SMAD2 mRNA expression but also protein expression. In addition, we detected the expression of miR-425 in ESCC tissues and plasma. Moreover, we analyzed the relationship between miR-425 expression and SMAD2 m RNA expression. We found that miR-425 was overexpressed in ESCC tissues and the plasma relative to adjacent normal tissues and plasma of healthy individuals. Furthermore, there was a negative correlation between miR-425 expression and SMAD2. Taken together, our results show that miR-425 functions as an oncogene by targeting the 30-UTR of SMAD2 and indicate the potential utility of plasma miR-425 as a novel biomarker for ESCC diagnosis. | Lingyan Liu Zitong Zhao Wei Zhou Xinyi Fan Qimin Zhan Yongmei Song | 2015 | Journal of Genetics and Genomics2015，42，11： | 10 |
| 8 | Lithospheric Stretching,Subsidence and Thermal History Modeling: Application to Yinggehai,Qiongdongnan and Songliao Basins in East China显示文摘LithosphericStretching,SubsidenceandThermalHistoryModeling:ApplicationtoYinggehai,QiongdongnanandSongliaoBasinsinEastChina*Li... | Lin ChangsongDepartment of Energy Resources, China University of Geosciences, Beijing 100083Li SitianFaculty of Earth Resources, China University of Geosciences, Wuhan 430074Zhang QiminWest Nanhai Oil Company, Zhanjiang 524000Zhang | 1997 | Journal of Earth Science1997，16，1： | 9 |
| 9 | TRAP1 Shows Clinical Significance and Promotes Cellular Migration and Invasion through STAT3/MMP2 Pathway in Human Esophageal Squamous Cell Cancer显示文摘Tumor necrosis factor receptor-associated protein 1(TRAP1), an important member of mitochondrial heat shock protein 90 family, is involved in multiple biological processes in several types of tumors. However, its pathological role in esophageal squamous cell cancer(ESCC) remains unknown. Herein, we demonstrated the clinical value of TRAP1, and its role in apoptosis and motility in ESCC. The clinical potential of TRAP1 was investigated through immunohistochemical analysis in 328 ESCC samples, which revealed that strong TRAP1 expression was associated with increased risk of lymph node metastasis, while high TRAP1 expression correlated with poor prognosis. Expression of TRAP1 was found to be an independent prognostic factor for patients with ESCC. Additionally, the upregulation of TRAP1 antagonized cisplatin-induced apoptosis while its downregulation sensitized cells to cisplatin-induced apoptosis. As revealed by the transwell assay, TRAP1 overexpression promoted cellular migration and invasion as compared to the control groups. In contrast,silencing of endogenous TRAP1 expression attenuated the ability of migration and invasion. Finally, the molecular mechanism investigated in the present study demonstrated that TRAP1-mediated migration and invasion occurred through STAT3/MMP2 signaling pathway. In conclusion, TRAP1 may be considered as a molecular predictive marker for prognosis and a novel molecular candidate for therapeutic target in ESCC. | Yunwei Ou Lingyan Liu Liyan Xue Wei Zhou Zitong Zhao Bainan Xu Yongmei Song Qimin Zhan | 2014 | Journal of Genetics and Genomics2014，41，10： | 8 |
| 10 | BAALC-AS1/G3BP2/c-Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma显示文摘Background:Long non-codingRNAs(lncRNAs)have been found to be involved in the development of many cancers.In this study,we aimed to identify the molecular mechanisms of lncRNA BAALC antisense RNA 1(BAALC-AS1)in regulating the malignancy of esophageal squamous cell carcinoma(ESCC).Methods:The expression of BAALC-AS1 in cancer patients was analyzed using a tissue microarray.The protein and RNA levels of BAALC-AS1 were determined by Western blotting analysis and quantitative reverse transcription-PCR(RT-qPCR),respectively.The cell proliferation was determined by cell viability assays,bromodeoxyuridine incorporation,and flow cytometry.The relationships among BAALC-AS1,RasGAPSH3 domain-binding protein 2(G3BP2),and c-Myc were determined using RNA immunoprecipitation,RNA pull-down assays,and luciferase assays.Results:The expression of BAALC-AS1 was highly up-regulated and associated with malignant phenotypes in ESCC tissues and cell lines.In vivo and in vitro assays showed that BAALC-AS1 promoted ESCC cell proliferation,migration,and invasion.BAALC-AS1 directly interacted with G3BP2,and thereby inhibited the degradation of c-Myc RNA 3’-UTR by G3BP2,thus leading to the accumulation of c-Myc expression.Additionally,c-Myc acted as a transcription factor that can induce the expression of BAALC-AS1 by directly binding to its promoter region.Conclusions:BAALC-AS1/G3BP2/c-Myc feedback loop plays a critical role in the development of ESCC,which might provide a novel therapeutic target and facilitate the development of new therapeutic strategies for the treatment of ESCC. | Hongyue Zhang Yan Wang Weimin Zhang Qingnan Wu Jiawen Fan Qimin Zhan | 2021 | Cancer Communications2021，41，3： | 7 |
| 11 | Migfilin promotes migration and invasion in glioma by driving EGFR and MMP-2 signalings:A positive feedback loop regulation显示文摘Glioma is the most common type of primary brain tumors in the central nervous system(CNS). Migfilin occurs in human glioma and enhances cellular motility via the epidermal growth factor receptor(EGFR)pathway. However, the underlying molecular mechanism is not fully understood. In this study, we found that Migfilin promoted matrix metalloproteinase-2(MMP-2) activity, and restrained the expression of tissue inhibitor of metalloproteinase 2(TIMP2), which is an MMP-2 inhibitor. Functional and structural studies showed that the LIM1 domain of Migfilin was required for Migfilin-mediated TIMP2 expression inhibition and MMP-2 activity, and was also necessary in promoting cell motility. Furthermore, Migfilininduced EGFR phosphorylation was greatly reduced by MMP-2 inhibitor(GM6001) or si RNA, while Migfilin-induced MMP-2 activation was also blocked by the EGFR inhibitor(AG1478) or si RNA. MMP-2 and EGFR inhibitors and their si RNAs can block Migfilin-induced migration and invasion, respectively.These results demonstrated that EGFR and MMP-2 signalings may form a positive feedback loop to enhance Migfilin-induced migration and invasion. Finally, we detected that the expression of Migfilin,EGFR phosphorylation(Tyr1173) and MMP-2 activity had a positive correlation in the clinical glioma sample. Taken together, these results suggest that Migfilin is a critical regulator in cellular motility by driving the EGFR-MMP-2 feedback loop, and may be considered as a potential therapeutic target in glioma. | Yunwei Ou Qingnan Wu Chuanyue Wu Xuefeng Liu Yongmei Song Qimin Zhan | 2017 | Journal of Genetics and Genomics2017，44，12： | 7 |
| 12 | FAT1, a direct transcriptional target of E2F1, suppresses cell proliferation, migration and invasion in esophageal squamous cell carcinoma显示文摘Objective: Growing evidence indicates that FAT atypical cadherin 1(FAT1) has aberrant genetic alterations and exhibits potential tumor suppressive function in esophageal squamous cell carcinoma(ESCC). However, the role of FAT1 in ESCC tumorigenesis remains not well elucidated. The aim of this study was to further investigate genetic alterations and biological functions of FAT1, as well as to explore its transcriptional regulation and downstream targets in ESCC.Methods: The mutations of FAT1 in ESCC were achieved by analyzing a combined study from seven published genomic data, while the copy number variants of FAT1 were obtained from an analysis of our previous data as well as of The Cancer Genome Atlas(TCGA) and Cancer Cell Line Encyclopedia(CCLE) databases using the cBioPortal. The transcriptional regulation of FAT1 expression was investigated by chromatin immunoprecipitation(ChIP) and the luciferase reporter assays. In-cell western, Western blot and reverse transcription-quantitative polymerase chain reaction(RT-qPCR) were used to assess the indicated gene expression. In addition, colony formation and Transwell migration/invasion assays were employed to test cell proliferation, migration and invasion.Finally, RNA sequencing was used to study the transcriptomes.Results: FAT1 was frequently mutated in ESCC and was deleted in multiple cancers. Furthermore, the transcription factor E2 F1 occupied the promoter region of FAT1, and depletion of E2 F1 led to a decrease in transcription activity and mRNA levels of FAT1. Moreover, we found that knockdown of FAT1 promoted KYSE30 and KYSE150 cell proliferation, migration and invasion;while overexpression of FAT1 inhibited KYSE30 and KYSE410 cell proliferation, migration and invasion. In addition, knockdown of FAT1 led to enrichment of the mitogen-activated protein kinase(MAPK) signaling pathway and cell adhesion process.Conclusions: Our data provided evidence for the tumor suppressive function of FAT1 in ESCC cells and elucidated the transcriptional regulation of FAT1 by E2 F1, which may facilitate the understanding of molecular mechanisms of the progression of ESCC. | Yu Wang Guangchao Wang Yunping Ma Jinglei Teng Yan Wang Yongping Cui Yan Dong Shujuan Shao Qimin Zhan Xuefeng Liu | 2019 | Chinese Journal of Cancer Research2019，31，4： | 6 |
| 13 | Chromosome analysis of esophageal squamous cell carcinoma cell line KYSE 410-4 by repetitive multicolor fluorescence in situ hybridization显示文摘Chromosome aberrations are distinctive features of human malignant tumors. Analysis of chromosomal changes can illuminate the molecular mechanisms underlying the development and progression of cancer. To establish the technique of multicolor fluorescence in situ hybridization (M-FISH) for identifying chromosome aberrations in esophageal carcinoma cell line KYSE 410-4, four pools of 6-color whole-chromosome painting probes have been designed and hybridized on the same metaphase spread by four rounds of repetitive FISH. Repetitive 6-color M-FISH was successfully established and the cytogenetic abnormalities in KYSE 410-4 cells were characterized. Chromosome gains occurred at 2q, 3, 8, 17p, and X. An isochromosome 3q was visualized in the cell line, which might be one intermedi- ate mechanism leading to 3p losses and/or 3q gains. Furthermore, 16 structural arrangements were detected, including four derivative chromosomes. The rearrangement of the centromeric regions accounted for approximately 44% of all rearrangements. The results added a more complete and accurate information of the genetic alterations to the classical cytogenetic description of KYSE 410-4 and provided a detailed cytogenetic background data for appropriate use of the cell line. The established 6-color M-FISH was useful for analyzing chro- mosomes in the whole genome of human tumors. | Yiling Yang Jiayou Chu Yupeng Wu Manli Luo Xin Xu Yaling Han Yan Cai Qimin Zhan Mingrong Wang | 2008 | Journal of Genetics and Genomics2008，35，1： | 6 |
| 14 | Analysis of microscopic pore structures of rocks before and after water absorption显示文摘岩石的吸水的特征被他们的显微镜的毛孔结构影响,它清楚地在水吸收以后变化。水吸收测试和扫描电子显微镜(SEM ) 在岩石上试验样品,在西藏在一个地点定位了,中国,被执行。在水吸收前后的岩石毛孔结构的变化与毛孔尺寸的分发和毛孔的分数维的特征被学习。因为新小毛孔的数字生产了,表面孔,毛孔的分数维的尺寸和毛孔结构的复杂性增加了的结果表演增加了或在岩石吸收了水以后,原来的 macropore 流动隧道被扩展。有他们的水吸收曲线上的变化的点。在另外的岩石的水吸收以后,当原来的毛孔流动隧道变得充满,表面孔和毛孔的分数维的尺寸和毛孔结构的复杂性减少了。水吸收曲线没变化。表面孔和岩石的毛孔分数维图形尺寸在水吸收前后有好线性关系。 | Li Dejian Wang Guilian Han Liqiang Liu Peiyu He Manchao Yang Guoxing Tai Qimin Chen Cheng | 2011 | Mining Science and Technology2011，21，2： | 6 |
| 15 | Downregulation of miR-503 Promotes ESCC Cell Proliferation,Migration,and Invasion by Targeting Cyclin D1显示文摘Esophageal squamous cell carcinoma(ESCC) is one of the most aggressive cancers in China,but the underlying molecular mechanism of ESCC is still unclear.Involvement of microRNAs has been demonstrated in cancer initiation and progression.Despite the reported function of miR-503 in several human cancers,its detailed anti-oncogenic role and clinical significance in ESCC remain undefined.In this study,we examined miR-503 expression by q PCR and found the downregulation of miR-503 expression in ESCC tissue relative to adjacent normal tissues.Further investigation in the effect of miR-503 on ESCC cell proliferation,migration,and invasion showed that enhanced expression of miR-503 inhibited ESCC aggressive phenotype and overexpression of CCND1 reversed the effect of miR-503-mediated ESCC cell aggressive phenotype.Our study further identified CCND1 as the target gene of miR-503.Thus,miR-503 functions as a tumor suppressor and has an important role in ESCC by targeting CCND1. | Lanfang Jiang Zitong Zhao Leilei Zheng Liyan Xue Qimin Zhan Yongmei Song | 2017 | Genomics, Proteomics & Bioinformatics2017，15，3： | 5 |
| 16 | Cdk phosphorylation licenses Kif4A chromosome localization required for early mitotic progression显示文摘 | Zhixiong Dong Changjun Zhu Qimin Zhan Wei Jiang | 2018 | Journal of Molecular Cell Biology2018，10，4： | 5 |
| 17 | Eigen microstates and their evolutions in complex systems显示文摘Emergence refers to the existence or formation of collective behaviors in complex systems.Here,we develop a theoretical framework based on the eigen microstate theory to analyze the emerging phenomena and dynamic evolution of complex system.In this framework,the statistical ensemble composed of M microstates of a complex system with N agents is defined by the normalized N×M matrix A,whose columns represent microstates and order of row is consist with the time.The ensemble matrix A can be decomposed as■,where r=min(N,M),eigenvalueσIbehaves as the probability amplitude of the eigen microstate U_I so that■and U_I evolves following V_I.In a disorder complex system,there is no dominant eigenvalue and eigen microstate.When a probability amplitudeσIbecomes finite in the thermodynamic limit,there is a condensation of the eigen microstate UIin analogy to the Bose–Einstein condensation of Bose gases.This indicates the emergence of U_I and a phase transition in complex system.Our framework has been applied successfully to equilibrium threedimensional Ising model,climate system and stock markets.We anticipate that our eigen microstate method can be used to study non-equilibrium complex systems with unknown orderparameters,such as phase transitions of collective motion and tipping points in climate systems and ecosystems. | Yu Sun Gaoke Hu Yongwen Zhang Bo Lu Zhenghui Lu Jingfang Fan Xiaoteng Li Qimin Deng Xiaosong Chen | 2021 | Communications in Theoretical Physics2021，73，6： | 5 |
| 18 | MiR-205 inhibits the invasion and migration of esophageal squamous cell carcinoma by modulating SMAD1 expression显示文摘Esophageal squamous cell carcinoma(ESCC)is one of the most lethal cancers worldwide.In this study,we aimed to investigate the underlying mechanisms of metastasis inhibition by miR-205 in ESCC.In microRNA(miRNA)array and quantitative RT-PCR analyses,we found that the expression level of miR-205 was significantly lower in patients with lymph node metastasis compared with that in patients without lymph node metastasis.After transfection of miR-205 mimics or inhibitors into ESCC cell lines,a significant negative correlation was observed between the expression level of miR-205 and Smad1.In luciferase reporter assays,we revealed that miR-205 inhibited the expression of SMAD1 by targeting the 30untranslated region(30-UTR)of SMAD1 mRNA in ESCC cells.Furthermore,our results showed that miR-205 suppressed the invasion and migration of ESCC cells,whereas Smad1 increased their invasion and migration.Taken together,our study demonstrates that miR-205 functions as a suppressor of tumor metastasis by regulating SMAD1expression through targeting the 30-UTR of SMAD1 mRNAin ESCC.Therefore,miR-205 may be a potential therapeutic target for miRNA-based therapy of ESCC. | Baoyu Liang Yan Wu Xu Han Xiaofei Zheng Qimin Zhan Tong Tong | 2014 | Chinese Science Bulletin2014，59，19： | 4 |
| 19 | Dynamic analysis of DNA damage induced miRNAs in colon cancer cells显示文摘It is known that microRNAs(miRNAs)expression profile shows substantial changes in cells under DNA damage.Here,we did miRNA microarray and quantitative real-time PCR to comprehensively identify the differentially expressed miRNAs in colon cancer cell lines HCT116 p53/and HCT116 p53-/-.Cluster analysis revealed a panel of differentially expressed miRNAs which are regulated by p53and/or UV-C induced DNA damage.These altered miRNAs tend to be located in chromosomes 13,X and 17.Moreover,pathways enrichment analysis estimated that MAPK pathway,focal adheren pathway,p53 pathway and Wnt pathway were mediated by these miRNAs to exert their functions in DNA damage response.Additionally,we found that miR-320a,one of the UV-C induced miRNAs,play a role in protecting cells from DNA damage.Taken together,our results show that miRNAs are dynamic regulated in p53-dependent or-independent manners in different cell contexts and different situations following DNA damage. | Weimin Zhang Fang Yang Qimin Zhan | 2014 | Chinese Science Bulletin2014，59，19： | 4 |
| 20 | Bioinformatic exploration of MTAl-regulated gene networks in colon cancer显示文摘 | Chunxiao Li Haijuan Wang Feng Lin Hui Li Tao Wen Haili Qian Qimin Zhan | 2016 | Frontiers of Medicine2016，10，2： | 4 |
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