3篇
您的检索式：作者名="Guixiong Fan"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | SETD8 induces stemness and epithelial–mesenchymal transition of pancreatic cancer cells by regulating ROR1 expression显示文摘Pancreatic cancer(PC)is one of the most deadly diseases,and its incidence is increasing year by year.The methyltransferase SETD8 has been demonstrated to play an important role in tumor cell proliferation and metastasis.However,little is known about whether SETD8 could affect the invasion and metastasis of PC and the mechanism underlying the regulation.Based on our previous report,here,we further found that SETD8 could promote the invasion and migration of PC cells by inducing the expression of receptor tyrosine kinase-like orphan receptor 1(ROR1).ROR1 was predominantly upregulated in PC tissues and was correlated with lymph node metastasis and worse prognosis.Mechanistically,SETD8 mediated ROR1 activity and regulated PC cells invasion and migration,although promoting the expression of stemness and epithelial–mesenchymal transition-related molecules.This promotion effect disappeared when the catalytically inactive mutant SETD8 was overexpressed,which could be counteracted by the SETD8-specific methyltransferase inhibitor UNC0379.Collectively,our results demonstrate that SETD8 may be a novel prognostic factor and a therapeutic target of PC. | Mengqi Liu Yihua Shi Qiangsheng Hu Yi Qin Shunrong Ji Wensheng Liu Qifeng Zhuo Guixiong Fan Zeng Ye Changfeng Song Xianjun Yu Xiaowu Xu Wenyan Xu | 2021 | Acta Biochimica et Biophysica Sinica2021，53，12： | 2 |
| 2 | FGFBPI-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer显示文摘Fibroblast growth factor-binding protein 1(FGFBP1)promotes fibroblast growth factor(FGF)activity by releasing FGFs from extracellular matrix storage.We previously reported that the tumor suppressor F-box and WD repeat domain-containing 7 suppresses FGFBP1 by reducing expression of c-Myc,which inhibits the proliferation and migration of pancreatic cancer cells.However,the potential mechanism by which FGFBP1 facilitates pancreatic ductal adenocarcinoma(PDAC)remains unexplored.In this study,we focused on the function of FGFBP1 in the interplay between cancer-associated fibroblasts(CAFs)and pancreatic cancer cells(PCCs).Decreased FGF22 expression was detected in CAFs co-cultured with PCCs with FGFBP1 abrogation,which was verified in the cell culture medium by enzyme-linked immunosorbent assay.Active cytokine FGF22 significantly facilitated the migration and invasion of PANC-1 and Mia PaCa-2 cells.The number of penetrating PCCs cocultured with CAFs with FGF22 abrogation was significantly less than that of the control group.Interestingly,higher expressions of FGF22 and fibroblast growth factor receptor 2(FGFR2)were associated with worse prognosis of patients with PDAC and FGFR2,an independent prognostic marker of PDAC.The PANC-1 and Mia PaCa-2 cells with silenced FGFR2 showed weaker invasion and metastasis,even if these cells were simultaneously treated with cytokine FGF22.These results revealed that FGFBPI-mediated interaction between CAFs and PCCs via FGF22/FGFR2 facilitates the migration and invasion of PCCs.FGFR2 could act as a prognostic marker for patients with PDAC. | Zheng Zhang Yi Qin Shunrong Ji Wenyan Xu Mengqi Liu Qiangsheng Hu Zeng Ye Guixiong Fan Xianjun Yu Wensheng Liu Xiaowu Xu | 2021 | Acta Biochimica et Biophysica Sinica2021，53，8： | 2 |
| 3 | MEN1 promotes ferroptosis by inhibiting mTOR-SCD1 axis in pancreatic neuroendocrine tumors显示文摘Pancreatic neuroendocrine tumor(pNET)is the second most common malignant tumors of the pancreas.Multiple endocrine neoplasia 1(MEN1)is the most frequently mutated gene in pNETs and MEN1-encoded protein,menin,is a scaffold protein that interacts with transcription factors and chromatin-modifying proteins to regulate various signaling pathways.However,the role of MEN1 in lipid metabolism has not been studied in pNETs.In this study,we perform targeted metabolomics analysis and find that MEN1 promotes the generation and oxidation of polyunsaturated fat acids(PUFAs).Meanwhile lipid peroxidation is a hallmark of ferroptosis,and we confirm that MEN1 promotes ferroptosis by inhibiting the activation of mTOR signaling which is the central hub of metabolism.We show that stearoyl-coA desaturase(SCD1)is the downstream of MEN1-mTOR signaling and oleic acid(OA),a metabolite of SCD1,recues the lipid peroxidation caused by MEN1 overexpression.The negative correlation between MEN1 and SCD1 is further verified in clinical specimens.Furthermore,we find that BON-1 and QGP-1 cells with MEN1 overexpression are more sensitive to everolimus,a widely used drug in pNETs that targets mTOR signaling.In addition,combined use everolimus with ferroptosis inducer,RSL3,possesses a more powerful ability to kill cells,which may provide a new strategy for the comprehensive therapy of pNETs. | Zeng Ye Haidi Chen Shunrong Ji Yuheng Hu Xin Lou Wuhu Zhang Desheng Jing Guixiong Fan Yue Zhang Xuemin Chen Qifeng Zhuo Jie Chen Xiaowu Xu Xianjun Yu Jin Xu Yi Qin Heli Gao | 2022 | Acta Biochimica et Biophysica Sinica2022，54，11： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员