2019•Molecular Medicine ReportsOpen access

miR‑221‑3p promotes the cell growth of non‑small cell lung cancer by targeting p27

Guo-Qing Yin, Bo Zhang, Jia Li

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Abstract

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.

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What this paper is about

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.

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Available abstract

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.

Key concepts: Cell cycle, Oncogene, microRNA, Cell growth, Biology, Downregulation and upregulation, Regulator, Cell

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