Long non‑coding RNA MIAT promotes gastric cancer proliferation and metastasis via modulating the miR‑331‑3p/RAB5B pathway
Author(s) -
Xiaomei Li,
Yanyan Jiao,
Bao-Hong Luan,
Hongxia Wu,
Rongrong Wang,
Jie Zhong
Publication year - 2020
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2020.12219
Subject(s) - gene knockdown , long non coding rna , apoptosis , oncogene , cancer research , cell growth , cell cycle , biology , metastasis , chemistry , microbiology and biotechnology , downregulation and upregulation , cancer , gene , biochemistry , genetics
Gastric cancer (GC) remains a threat to the health of the global population. The present study investigated the effects and mechanisms of the long non-coding RNA myocardial infarction associated transcript (MIAT) on the proliferation, apoptosis and metastasis of GC (HGC-27 and AGS) cells. The expression levels of MIAT, micoRNA (miR)-331-3p and RAB5B mRNA were analyzed using reverse transcription-quantitative PCR analysis. Cell growth, apoptosis, migration and invasion were measured using 5-ethynyl-2′-deoxyuridine, flow cytometry, wound healing and Transwell assays, respectively. A luciferase assay was used to determine whether miR-331-3p targeted MIAT and RAB5B. The results indicated that MIAT levels were significantly upregulated in GC tissues and cells, correlated with RAB5B levels and inversely associated with miR-331-3p levels. MIAT overexpression promoted proliferation and metastasis, and inhibited the apoptosis of GC cells . MIAT knockdown had the opposite effect on GC cells . The rescue experiments revealed that the effects of MIAT knockdown on the biological behaviour of GC cells were attenuated by RAB5B overexpression. These data suggest that MIAT promotes GC progression via modulating miR-331-3p/RAB5B pathway.
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