USP52 inhibits cell proliferation by stabilizing PTEN protein in non-small cell lung cancer | Zendy

Maoshu Zhu | Zendy; Hui Zhang | Zendy; Fuhua Lu | Zendy; Zhaowei Wang | Zendy; Yulong Wu | Zendy; Huoshu Chen | Zendy; Xin Fan | Zendy; Zhijiang Yin | Zendy; Fulong Liang | Zendy

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USP52 inhibits cell proliferation by stabilizing PTEN protein in non-small cell lung cancer

Author(s) -

Maoshu Zhu,

Hui Zhang,

Fuhua Lu,

Zhaowei Wang,

Yulong Wu,

Huoshu Chen,

Xin Fan,

Zhijiang Yin,

Fulong Liang

Publication year - 2021

Publication title -

bioscience reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.938

H-Index - 77

eISSN - 1573-4935

pISSN - 0144-8463

DOI - 10.1042/bsr20210486

Subject(s) - pten , tensin , lung cancer , cancer research , cyclin d1 , pi3k/akt/mtor pathway , cell growth , protein kinase b , cancer , biology , ubiquitin , suppressor , cell , cell cycle , signal transduction , medicine , microbiology and biotechnology , biochemistry , gene

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer. Ubiquitination is closely related to the development of lung cancer. However, the biological importance of newly discovered ubiquitin-specific peptidase (USP) 52 (USP52) in NSCLC remained unclear. Here, our findings identify USP52 as a novel tumor suppressor of NSCLC, the low expression of USP52 predicts a poor prognosis for NSCLC patients. The present study demonstrates that USP52 inhibits cancer cell proliferation through down-regulation of cyclin D1 (CCND1) as well as AKT/mTOR signaling pathway inhibition. Meanwhile, USP25 also suppresses NSCLC progression via enhancing phosphatase and tensin homolog (PTEN) stability in cancer cells, which further indicates the significance/importance of USP52 in NSCLC suppression.

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