Abstract
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.
Highlights
Gastric cancer (GC) is a common cancer worldwide and ranks third among the leading causes of cancer‐associated mortalities
RT‐qPCR results revealed that myocardial infarction associated transcript (MIAT) expression was signifi‐ cantly increased in GC tissue samples as compared with paratumor tissues (Fig. 1A)
MIAT was revealed to be upregulated in GC tissues, which is consistent with previous reports [25]
Summary
Gastric cancer (GC) is a common cancer worldwide and ranks third among the leading causes of cancer‐associated mortalities. Incidence rates are markedly elevated in Eastern Asia (incidence rates are 24.7 per 100,000), when compared with Northern America (incidence rates are 8.4 per 100,000) and Northern. Targeted therapy with biomarkers for advanced GC has developed rapidly in recent years [2]. Patients with extensive invasion and metastasis have poor prognoses [3]. Even after a complete resection, recurrence occurs in ~50% of patients [4]. As the molecular mechanisms underlying the metastasis and recurrence of GC have not been fully clarified, identifying key GC‐promoting molecules may contribute to the understanding of GC pathogenesis and identification of new therapeutic targets
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