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Am J Cancer Res. 2017 Sep 1;7(9):1820-1834. eCollection 2017.

HOXC13 promotes proliferation of lung adenocarcinoma via modulation of CCND1 and CCNE1.

Author information

1
Department of Respiratory Medicine, Nanjing Chest Hospital, Medical School of Southeast UniversityNanjing, Jiangsu, China.
2
Medical School of Southeast UniversityNanjing, Jiangsu, China.
3
Department of Cardiothoracic Surgery, Jinling Hospital, Medical School of Nanjing UniversityNanjing, Jiangsu, China.
4
Department of Cardiothoracic Surgery, Jinling Hospital, Southern Medical UniversityNanjing, Jiangsu, China.

Abstract

In this study, we confirmed that HOXC13 might be a potential oncogene in lung adenocarcinoma through an analysis of The Cancer Genome Atlas (TCGA) datasets. Further analysis revealed that the expression of HOXC13 was significantly higher in lung adenocarcinoma tissues than in adjacent normal tissues; importantly, its expression correlated with poor clinical characteristics and worse prognosis. In vitro experiments showed that HOXC13 expression generally increased in lung adenocarcinoma cell lines. Moreover, knockdown of HOXC13 inhibited lung adenocarcinoma cell proliferation, and induced G1-phase arrest via downregulation of CCND1 and CCNE1. Conversely, HOXC13 overexpression promoted lung adenocarcinoma cell proliferation, and decreased the percentage of cells in G1-phase via upregulation of CCND1 and CCNE1. We also found that miR-141 downregulated HOXC13, by directly targeting its 3'UTR, and inhibited proliferation of lung adenocarcinoma cells. Taken together, our results suggest that HOXC13, which is directly targeted by miR-141, is highly expressed in lung adenocarcinoma, and promotes proliferation of lung adenocarcinoma by modulating the expression of CCND1 and CCNE1.

KEYWORDS:

CCND1; CCNE1; HOXC13; lung adenocarcinoma; miR-141

PMID:
28979806
PMCID:
PMC5622218

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