microRNA-363-3p inhibits cell growth and invasion of non‑small cell lung cancer by targeting HMGA2

Lung cancer is the second most common cancer and is the leading cause of cancer-related death worldwide. For decades, increasing evidence revealed that microRNAs may contribute to non‑small cell lung cancer (NSCLC) carcinogenesis and progression and could provide novel therapeutic targets for treatm...

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Veröffentlicht in:Molecular medicine reports 2018-02, Vol.17 (2), p.2712-2718
Hauptverfasser: Jiang, Chuanfu, Cao, Yang, Lei, Ting, Wang, Yu, Fu, Junfeng, Wang, Ze, Lv, Zhenyang
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Sprache:eng
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Zusammenfassung:Lung cancer is the second most common cancer and is the leading cause of cancer-related death worldwide. For decades, increasing evidence revealed that microRNAs may contribute to non‑small cell lung cancer (NSCLC) carcinogenesis and progression and could provide novel therapeutic targets for treatments of patients with NSCLC. Accumulated studies indicate that microRNA (miR)‑363‑3p serves important roles in tumorigenesis and tumor development; however, the role of miR‑363‑3p in NSCLC is still unclear. The current study reported that miR‑363‑3p exhibited reduced expression in NSCLC tissues and cell lines. Reduced miR‑363‑3p expression was correlated with tumor node metastasis classification and distant metastasis of NSCLC patients. Notably, miR‑363‑3p re‑expression significantly suppressed cell proliferation and invasion of NSCLC. Furthermore, bioinformatics analysis, luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blotting indicated that (high mobility group AT-hook 2) HMGA2 was a direct target gene of miR‑363‑3p. HMGA2 was increased in NSCLC tissues and inversely associated with HMGA2 expression. Moreover, HMGA2 underexpression had similar effects to miR‑363‑3p overexpression in NSCLC cells. Thus, the current study suggested that miR‑363‑3p may act as a tumor suppressor in NSCLC and that the miR‑363‑3p could be investigated as a therapeutic target for the patients with this disease.
ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2017.8131