Emerging evidence suggests the critical function of microRNAs in regulating the growth of cancer cells. In the present study, it was demonstrated that miR-221-3p was overexpressed in non-small cell lung cancer (NSCLC) tissues and cell lines compared with that noted in the normal controls. Downregulation of miR-221-3p suppressed the proliferation, colony formation and invasion of NSCLC cells. To further understand the molecular mechanisms underlying the potential oncogenic function of miR-221-3p in NSCLC, the downstream targets of miR-221-3p were predicted using bioinformatic databases. The prediction suggested the cell cycle regulator p27 as one of the targets of miR-221-3p. Molecular experiments showed that miR-221-3p was able to bind with the 3′-untranslated region (UTR) of p27 and decreased the expression of p27 in NSCLC cells. Consistent with the suppressive role of p27 in controlling cell cycle progression, overexpression of miR-221-3p decreased the expression of p27 and promoted cell cycle progression from G1 to S phase. Collectively, our findings identified miR-221-3p as a novel regulator of NSCLC cell growth via modulating the expression of p27.
Gastric cancer (GC) is the fourth leading cause of cancer-related death. The occurrence and development of GC is a complex process involving multiple biological mechanisms. Although traditional regulation modulates molecular functions related to the occurrence and development of GC, the comprehensive mechanisms remain unclear. Ultraconserved region (UCR) refers to a genome sequence that is completely conserved in the homologous regions of the human, rat and mouse genomes, with 100% identity, without any insertions or deletions, and often located in fragile sites and tumour-related genes. The transcribed UCR (T-UCR) is transcribed from the UCR and is a new type of long noncoding RNA. Recent studies have found that the expression level of T-UCRs changes during the occurrence and development of GC, revealing a new mechanism underlying GC. Therefore, this article aims to review the relevant research on T-UCRs in GC, as well as the function of T-UCRs and their regulatory role in the occurrence and development of GC, to provide new strategies for GC diagnosis and treatment.
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