3篇
您的检索式：作者名="Guangchen ZU"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | MicroRNA-708 inhibits the proliferation and chemoresistance of pancreatic cancer cells显示文摘Pancreatic cancer is one of the most aggressive malignancies with poor prognosis and high mortality.Recent studies showed that microRNAs are dysregulated and involved in the initiation and progression of pancreatic cancer.In this study,we found that miR-708 was significantly downregulated in pancreatic cancer tissues and cell lines.Lentivirus-mediated overexpression of miR-708 could significantly inhibit the proliferation and invasion,while enhanced chemosensitivity to gemcitabine in both Panc-1 and SW1990 cells.Luciferase reporter assay showed that miR-708 bound the 3’-untranslated region of survivin and suppressed the expression of survivin in pancreatic cancer cells.In pancreatic cancer tissues,survivin protein was highly expressed and negatively correlated with miR-708 expression.Furthermore,the restoration of survivin expression could partially antagonize proliferation inhibition and apoptosis induction by miR-708 in pancreatic cancer cells.The Panc-1 cells with overexpression of miR-708 also showed decreased proliferation capability in nude mouse model compared with parental cells.In conclusion,our results suggest that miR-708 inhibits pancreatic cancer and could be a novel potential candidate to treat pancreatic cancer. | Wensong LIU Yunjie LU Dong ZHANG Longqing SHI Guangchen ZU Haijiao YAN Donglin SUN | 2020 | BIOCELL2020，44，1： | 1 |
| 2 | PITX2 in pancreatic stellate cells promotes EMT in pancreatic cancer cells via the Wnt/β-catenin pathway显示文摘Since the prognosis of patients with pancreatic cancer is very poor and there is a lack of treatment methods,this study is performed to investigate the function of PITX2 in pancreatic stellate cells(PSCs)in the progression of pancreatic cancer.Scientific hypotheses are proposed according to bioinformatics analysis and tissue microarray analysis.Stable knockdown of PITX2 in PSCs is achieved through lentiviral infection.The relative expressions of PITX2,α-SMA,vimentin,CTNNB1,AXIN1 and LEF1 are measured in wild-type PSCs and PITX2-knockdown PSCs.Proliferative capacity is measured by EdU assay.After coculture with PSCs,the proliferation,invasion and migration capacity of pancreatic cancer cells are tested.EMT and Wnt/β-catenin downstream genes of pancreatic cancer cells are investigated to reveal the potential mechanism.Bioinformatics analysis reveals that the PITX2 gene is highly expressed in stromal cells in pancreatic cancer and is correlated with squamous-type PDAC.Analysis of PDAC tissue microarray further demonstrates that high PITX2 level in stromal cells is correlated with poor prognosis in PDAC.After stable knockdown of PITX2 in PSCs,the relative protein levels ofα-SMA,vimentin,CTNNB1,AXIN1 and LEF1 are decreased,and the proliferative capacity of PSCs is also decreased.After coculture with PSCs,in which PITX2 expression is downregulated,the proliferation,invasion and migration capacities of pancreatic cancer cells are inhibited.Thus,our results show that PITX2-silenced PSCs inhibit the growth,migration and invasion of pancreatic cancer cells via reduced EMT and Wnt/β-catenin signaling. | Di Wu Weibo Chen Yang Yang Yi Qin Guangchen Zu Yue Zhang Yong An Donglin Sun Xiaowu Xu Xuemin Chen | 2023 | Acta Biochimica et Biophysica Sinica2023，55，9： | 1 |
| 3 | A positive feedback loop of ARF6 activates ERK1/2 signaling pathway via DUSP6 silencing to promote pancreatic cancer progression显示文摘ERK1/2 are essential proteins mediating mitogen-activated protein kinase signaling downstream of RAS in pancreatic adenocarcinoma(PDAC).Our previous study reveals that ARF6 plays a positive regulatory role in ERK1/2 pathway in a feedback loop manner.A significant part of the literature on ARF6 has emphasized its oncogenic effect as an essential downstream molecule of ERK1/2,and no research has been done on the regulation mechanisms of the feedback loop between ARF6 and the ERK1/2 signaling pathway.In the present study,we explore the gene network downstream of ARF6 and find that DUSP6 may be the critical signal molecule in the positive feedback loop between ARF6 and ERK1/2.Specifically,to elucidate the negative correlations between ARF6 and DUSP6 in pancreatic cancer,we examine their expressions in pancreatic cancer tissues by immunohistochemical staining.Then the impact of DUSP6 on the proliferation and apoptosis of PDAC cells are investigated by gain-of-function and loss-of-function approaches.Mechanism explorations uncover that ARF6 suppresses the expression of DUSP6,which is responsible for the dephosphorylation of ERK1/2.Altogether,these results indicate that DUSP6 plays a tumor-suppressive role and acts as an intermediate molecule between ARF6 and ERK1/2 in PDAC cells,thereby forming a positive feedback loop. | Bingkai Xiao Yue Zhang Zekun Lu Weibo Chen Yong An Guangchen Zu Xiaowu Xu Di Wu Hao Yang Yi Qin Xuemin Chen | 2022 | Acta Biochimica et Biophysica Sinica2022，54，10： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员