Open AccessLong non‐coding RNA CASC 15 regulates gastric cancer cell proliferation, migration and epithelial mesenchymal transition by targeting CDKN 1A and ZEB 1
Author(s) -
Wu Qiong,
Xiang Shihao,
Ma Jiali,
Hui Pingping,
Wang Ting,
Meng Wenying,
Shi Min,
Wang Yugang
Publication year - 2018
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1002/1878-0261.12187
Subject(s) - gene knockdown , carcinogenesis , biology , rna , cell growth , non coding rna , microbiology and biotechnology , chemistry , cell , cell cycle , cancer research , cancer , cell culture , gene , biochemistry , genetics
Long non‐coding RNA (lnc RNA ) is responsible for a diverse range of cellular functions, such as transcriptional and translational regulation and variance in gene expression. The lnc RNA CASC 15 (cancer susceptibility candidate 15) is a long intergenic non‐coding RNA (linc RNA ) locus in chromosome 6p22.3. Previous research shows that lnc RNA CASC 15 is implicated in the biological behaviors of several cancers such as neuroblastoma and melanoma. Here, we aimed to explore in detail how CASC 15 contributes to the growth of gastric cancer (GC). As predicted, the expression of CASC 15 was enriched in GC tissues and cell lines as compared with healthy tissues and cells using qRT ‐ PCR . The Kaplan–Meier method was used to demonstrate that high expression of CASC 15 is linked to a poor prognosis for patients suffering from GC. Additionally, functional experiments proved that the down‐ or up‐regulation of CASC 15 inhibited or facilitated cell proliferation via the induction of cell cycle arrest and apoptosis, and also suppressed or accelerated cell migration and invasion by affecting the progression of the epithelial‐to‐mesenchymal transition ( EMT ). In vivo experiments showed that the knockdown of CASC 15 lessened the tumor volume and weight and influenced the EMT process. This was confirmed by western blot assays and immunohistochemistry, indicating impaired metastatic ability in nude mice. CASC 15 involvement in the tumorigenesis of GC occurs when CASC 15 interacts with EZH 2 and WDR 5 to modulate CDKN 1A in nucleus. Additionally, the knockdown of CASC 15 triggered the silencing of ZEB 1 in cytoplasm, which was shown to be associated with the competitive binding of CASC 15 to miR‐33a‐5p.