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Biomed Pharmacother. 2019 Jun;114:108831. doi: 10.1016/j.biopha.2019.108831. Epub 2019 Apr 12.

Amplification of USP13 drives non-small cell lung cancer progression mediated by AKT/MAPK signaling.

Author information

1
The Second Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, PR China.
2
The Second Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, PR China; Molecular Physiology Division, Department of Zoology, Faculty of Science, Beni-Suef University, Egypt.
3
The Second Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, PR China. Electronic address: 1310991@qq.com.
4
The Second Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, PR China. Electronic address: liusy@dlmedu.edu.cn.

Abstract

USP13 is emerging as a potential target in cancer therapy. However, the effect of USP13 on tumor progression is controversial. Here we focused on non-small cell lung cancer (NSCLC), a common cancer with high mortality, and studied the role of USP13 in tumor growth. By analysis of multi-level genetic database, we found USP13 is high expressed in heart among healthy primary tissues and is most amplified in lung cancer. Clinical samples of NSCLC showed tumor exhibited high USP13 level compared with adjacent normal tissues. We further utilized lung adenocarcinoma A549 and squamous carcinoma H226 cells as cell model and investigated USP13 effect by USP13 knockdown. As a results, downregulation of USP13 dramatically inhibited A549 and H226 cell proliferation by AKT/MAPK signaling and suppressed tumor growth in nude mice. Collectively, we identified USP13 as a tumor promoter in NSCLC and provide a promising target in cancer therapy.

KEYWORDS:

AKT/MAPK signaling; Amplification; NSCLC; Tumor promoter; USP13

PMID:
30986623
DOI:
10.1016/j.biopha.2019.108831
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