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

Yue Wu, Yingqiu Zhang, Congcong Liu, Yang Zhang, Duchuang Wang, Shanshan Wang, Yueguang Wu, Fang Liu, Qiong Li, Xiuxiu Liu, Mohamed Y. Zaky, Dong Yan, Shuyan Liu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)

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.

Original languageEnglish
Article number108831
JournalBiomedicine and Pharmacotherapy
Volume114
DOIs
Publication statusPublished - Jun 2019
Externally publishedYes

Keywords

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

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