MiR-4733-5p promotes gallbladder carcinoma progression via directly targeting kruppel like factor 7

被引:7
|
作者
Hu, Xiaoqiang [1 ]
Zhang, Junzhe [1 ]
Bu, Junfeng [1 ]
Yang, Kaini [1 ]
Xu, Sunwang [1 ]
Pan, Mengqiao [1 ]
Xiang, Dongxi [1 ,2 ]
Chen, Wei [1 ,3 ,4 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Biliary & Pancreat Surg, Shanghai 200120, Peoples R China
[2] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Shanghai Canc Inst, Renji Hosp,Sch Med, Shanghai 200120, Peoples R China
[3] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Key Lab Biliary Tract Dis, Sch Med, Shanghai 200120, Peoples R China
[4] Shanghai Jiao Tong Univ, Shanghai Res Ctr Biliary Tract Dis, Renji Hosp, Sch Med, Shanghai 200120, Peoples R China
关键词
Gallbladder cancer; MiRNA; epithelial-mesenchymal transition; MiR-4733-5p; KLF7; EPITHELIAL-MESENCHYMAL TRANSITION; CANCER; METASTASIS; PLASTICITY; INSIGHTS; RNAS;
D O I
10.1080/21655979.2022.2065951
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Gallbladder carcinoma (GBC) is highly aggressive with poor prognosis. Accumulating reports show that miRNAs play critical roles in tumor progression. Previous studies have identified several miRNAs that promoted or inhibited GBC cell proliferation and/or metastasis. Here, we used the Gene Expression Omnibus (GEO) dataset to identify dysregulated miRNAs in GBC, followed by validating the upregulation of the miR-4733-5p and downregulation of kruppel-like factor 7 (KLF7) in GBC biopsies by quantitative real-time PCR (RT-qPCR), in situ hybridization (ISH) staining, and immunohistochemistry (IHC) assays. GBC cell proliferation and invasion capacities mediated by miR-4733-5p were evaluated by a series of function assays in vitro, including CCK-8, colony formation assay, wound healing assay and transwell assay. Xenograft tumor model found that miR-4733-5p promoted GBC tumor growth in vivo. This study clarified that miR-4733-5p was upregulated in GBC and promoted GBC cell proliferation via directly binding to 3' untranslated region (UTR) of KLF, which was downregulated and prohibited the proliferation and migration of GBC cells.
引用
收藏
页码:10691 / 10706
页数:16
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