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USP52 inhibits cell proliferation by stabilizing PTEN protein in non-small cell lung cancer.
Bioscience Reports ( IF 3.8 ) Pub Date : 2021-09-17 , DOI: 10.1042/bsr20210486
Maoshu Zhu 1, 2 , Hui Zhang 2, 3 , Fuhua Lu 2, 3 , Zhaowei Wang 2, 4 , Yulong Wu 2, 5 , Huoshu Chen 2, 6 , Xin Fan 7 , Zhijiang Yin 2, 5 , Fulong Liang 2, 3
Affiliation  

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 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. This study demonstrates that USP52 inhibits cancer cell proliferation through downregulation of cyclin D1 as well as AKT/mTOR signaling pathway inhibition. Meanwhile, USP25 also suppresses NSCLC progression via enhancing PTEN stability in cancer cells, which further indicates the significance/importance of USP52 in NSCLC suppression.

中文翻译:

USP52 通过稳定非小细胞肺癌中的 PTEN 蛋白来抑制细胞增殖。

非小细胞肺癌(NSCLC)是肺癌最常见的亚型。泛素化与肺癌的发生发展密切相关。然而,新发现的泛素特异性肽酶 52 (USP52) 在 NSCLC 中的生物学重要性仍不清楚。在此,我们的研究结果将 USP52 确定为 NSCLC 的新型肿瘤抑制因子,USP52 的低表达预示着 NSCLC 患者的不良预后。这项研究表明,USP52 通过下调 cyclin D1 以及抑制 AKT/mTOR 信号通路来抑制癌细胞增殖。同时,USP25还通过增强癌细胞中PTEN的稳定性来抑制NSCLC进展,这进一步表明了USP52在抑制NSCLC中的意义/重要性。
更新日期:2021-09-17
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