文章：

USP30通过稳定Snail促进乳腺癌进展

USP30 promotes the progression of breast cancer by stabilising Snail 

原文发布日期：2023-12-25 

英文摘要：

Breast cancer (BC) is the most prevalent tumour in women worldwide. USP30 is a deubiquitinase that has been previously reported to promote tumour progression and lipid synthesis in hepatocellular carcinoma. However, the role of USP30 in breast cancer remains unclear. Therefore, we investigated its biological action and corresponding mechanisms in vitro and in vivo. In our study, we found that USP30 was highly expressed in breast cancer samples and correlated with a poor patient prognosis. Knockdown of USP30 significantly suppressed the proliferation, invasion and migration abilities of BC cells in vitro and tumour growth in vivo, whereas overexpression of USP30 exhibited the opposite effect. Mechanistically, we verified that USP30 interacts with and stabilises Snail to promote its protein expression through deubiquitination by K48-linked polyubiquitin chains and then accelerates the EMT program. More importantly, USP30 reduced the chemosensitivity of BC cells to paclitaxel (PTX). Collectively, these data demonstrate that USP30 promotes the BC cell EMT program by stabilising Snail and attenuating chemosensitivity to PTX and may be a potential therapeutic target in BC. 

摘要翻译： 

乳腺癌（BC）是全球女性中最常见的肿瘤。USP30是一种去泛素化酶，既往研究报道其在肝细胞癌中能促进肿瘤进展和脂质合成。然而，USP30在乳腺癌中的作用尚不明确。为此，我们通过体外和体内实验探究了其生物学功能及相应作用机制。研究发现，USP30在乳腺癌样本中高表达，且与患者不良预后相关。敲低USP30可显著抑制BC细胞在体外的增殖、侵袭和迁移能力以及体内肿瘤生长，而过表达USP30则产生相反效应。从机制上，我们证实USP30通过与Snail相互作用，通过K48连接的多聚泛素链去泛素化稳定Snail蛋白表达，进而加速上皮间质转化（EMT）进程。更重要的是，USP30会降低BC细胞对紫杉醇（PTX）的化疗敏感性。综上所述，这些数据表明USP30通过稳定Snail蛋白促进BC细胞EMT进程并降低对PTX的化疗敏感性，可能成为BC治疗的潜在靶点。

原文链接：

USP30 promotes the progression of breast cancer by stabilising Snail