The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer

被引:98
作者
Wang, Shou-Hua [1 ]
Zhang, Wen-Jie [1 ]
Wu, Xiao-Cai [1 ]
Weng, Ming-Zhe [1 ]
Zhang, Ming-Di [1 ]
Cai, Qiang [1 ]
Di Zhou [1 ]
Wang, Jian-Dong [1 ]
Quan, Zhi-Wei [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Gen Surg, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
gallbladder cancer; MALAT1; competing endogenous RNA; miR-363-3p; MCL-1; MYELOID CELL LEUKEMIA-1; LONG NONCODING RNA; POOR-PROGNOSIS; DOWN-REGULATION; METASTASIS; PROMOTES; PREDICTS; CARCINOMA; APOPTOSIS;
D O I
10.1111/jcmm.12920
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Gallbladder carcinoma (GBC) is an aggressive neoplasm, and the treatment options for advanced GBC are limited. Recently, long non-coding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in several cancers. In this study, we found that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression was up-regulated in GBC tissues (P < 0.05). Luciferase reporter assays and RNA pull down assays showed that MALAT1 is a target of miR-363-3p. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells. Furthermore, MALAT1 silencing decreased GBC cell proliferation and the S phase cell population and induced apoptosis in vitro. In vivo, tumour volumes were significantly decreased in the MALAT1 silencing group compared with those in the control group. These data demonstrated that the MALAT1/miR-363-3p/MCL-1 regulatory pathway controls the progression of GBC. Inhibition of MALAT1 expression may be to a novel therapeutic strategy for gallbladder cancer.
引用
收藏
页码:2299 / 2308
页数:10
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