Colorectal cancer (CRC) is the third most common malignant disease globally and causes numerous cancer-associated mortalities; however, the underlying molecular mechanisms remain unresolved. MicroRNAs (miRs) are endogenous noncoding RNAs that… Click to show full abstract
Colorectal cancer (CRC) is the third most common malignant disease globally and causes numerous cancer-associated mortalities; however, the underlying molecular mechanisms remain unresolved. MicroRNAs (miRs) are endogenous noncoding RNAs that regulate post-transcriptional gene silencing by annealing to partially complementary sequences in the 3′-untranslated regions of target mRNAs. In the present study, expression of the tumor suppressor gene inhibitor of growth protein 4 (ING4) in cell lines was investigated using reverse transcription-quantitative polymerase chain reaction and western blotting. miR-650 overexpression promoted CRC cell proliferation and migration by targeting ING4 when the cells were transfected with the miR-650 mimics. Additionally, overexpression of miR-650 increased the epithelial-mesenchymal transition and activation of the Ras homolog gene family member A/Ras-related C3 botulinum toxin GTPase. Extracellular signal-regulated kinases and p38 mitogen-activated protein kinase signaling were markedly activated when miR-650 was increased in CRC cells. Combined, the results indicate the mechanism underlying the miR-650 promotion of CRC progression, and provide promising potential biomarkers for the prognosis and treatment of CRC.
               
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