Open AccessLong non‐coding RNA MYOSLID functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐29c‐3p in gastric cancer
Author(s) -
Han Yuying,
Wu Nan,
Jiang Mingzuo,
Chu Yi,
Wang Zhiyang,
Liu Hao,
Cao Jiayi,
Liu Hanming,
Xu Bing,
Xie Xin
Publication year - 2019
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12678
Subject(s) - competing endogenous rna , gene knockdown , microrna , biology , long non coding rna , carcinogenesis , cancer research , cancer , rna , regulator , oncomir , gene , genetics
Objective Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. Methods We investigate the biological function, mechanism of action and clinical expression of lncRNA MYOSLID in GC. First, we analysed the differential expression of lncRNA MYOSLID in GC tissues and non‐cancerous tissues by analysing the sequencing data obtained from The Cancer Genome Atlas. Subsequently, we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR‐29c‐3p. The nude mouse xenograft was used to further confirm the functional significance of lncRNA MYOSLID in vivo. Results We found for the first time that the expression of lncRNA MYOSLID was significantly up‐regulated in GC tissues, and the up‐regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. In addition, apoptosis and growth arrest can be induced in vitro after knockdown of lncRNA MYOSLID, which inhibits tumorigenesis in mouse xenografts in vivo. Further in‐depth studies revealed that lncRNA MYOSLID acts as a ceRNA of miR‐29c‐3p, resulting in de‐repression of its downstream target gene MCL‐1. Conclusion The lncRNA MYOSLID‐miR‐29c‐3p‐MCL‐1 axis plays a key role in the development of GC. Our findings may provide potential new targets for the diagnosis and treatment of human GC.