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lncRNA SNHG1 cooperated with miR‐497/miR‐195‐5p to modify epithelial–mesenchymal transition underlying colorectal cancer exacerbation
Author(s) -
Bai Jinghui,
Xu Jian,
Zhao Jian,
Zhang Rui
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29065
Subject(s) - epithelial–mesenchymal transition , colorectal cancer , exacerbation , transition (genetics) , microrna , cancer research , mesenchymal stem cell , cancer , biology , medicine , microbiology and biotechnology , gene , genetics
Our study was intended to provide evidence for whether long noncoding RNA (lncRNA) SNHG1 would accelerate the epithelial–mesenchymal transition (EMT) course intrinsic in colorectal cancer (CRC) by sponging downstream miR‐497‐5p and miR‐195‐5p. We altogether collected 338 pairs of CRC and noncancerous tissues, and meanwhile purchased five CRC cell lines (i.e., SW480, HCT116, Lovo, CaCO‐2, and HT29) and human embryo intestinal mucosal tissue‐sourced cell line (i.e., CCC‐HIE‐2). The CRC cells as mentioned above were appraised regarding their potencies in proliferation, migration, and invasion, after being transfected with pcDNA3.1‐SNHG1, si‐SNHG1, miR‐195‐5p mimic/inhibitor, and miR‐497‐5p mimic/inhibitor. Eventually, we depended on reverse transcription‐polymerase chain reaction to assess SNHG1, miR‐497‐5p, and miR‐195‐5p expressions, and the protein levels of EMT‐specific molecules were determined on the strength of western blotting. It seemed that there was a high potential for highly expressed SNHG1 and lowly expressed miR‐497/miR‐195 to symbolize CRC patients’ unfavorable prognosis ( p < .05). Concurrently, CRC cells were detected with higher SNHG1 expression and lower miR‐497/miR‐195 expression than CCC‐HIE‐2 cells ( p < .05). In addition, the EMT process of CRC cells was facilitated markedly against the contexts of overexpressed SNHG1 and underexpressed miR‐497‐5p/miR‐195‐5p. Intriguingly, the strength of miR‐195‐5p collaborating with miR‐497‐5p in affecting the activity of CRC cells seemed to overweigh that of miR‐497/miR‐195‐5p alone. Besides, both miR‐195‐5p and miR‐497‐5p were subjected to in vivo and in vitro modification of SNHG1 ( p < .05). Conclusively, application of lncRNA SNHG1 for treating CRC might be promising, given its dual modulation of miR‐497 and miR‐195 underlying CRC pathogenesis.