期刊
ONCOGENE
卷 41, 期 11, 页码 1589-1599出版社
SPRINGERNATURE
DOI: 10.1038/s41388-022-02204-1
关键词
-
资金
- National Natural Science Foundation of China [82003236]
- Zhejiang Provincial Nature Science Foundation of China [LY20H160044]
- Gansu Provincial National Science Foundation for Distinguished Young Scholars [21JR7RA389]
This study reveals that TRIM32 is upregulated and negatively associated with survival of TNBC patients. Radiotherapy enhances the expression of TRIM32, while depletion of TRIM32 reduces TNBC radioresistance. Mechanistically, radiotherapy promotes the association between TRIM32 and nuclear STAT3, which suppresses TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues and correlated with poor prognosis of TNBC patients.
Radioresistance is common in the treatment of triple-negative breast cancer (TNBC), but the molecular mechanisms involved remain unclear. Herein, we reveal that tripartite motif-containing protein 32 (TRIM32) is upregulated in TNBC and is negatively associated with survival of TNBC patients. Radiotherapy resulted in enhanced expression of TRIM32, whereas TRIM32 depletion reduced TNBC radioresistance in vitro and in vivo. Mechanistically, radiotherapy promoted the association between TRIM32 and nuclear STAT3, which suppressed TC45-induced dephosphorylation of STAT3, resulting in increased STAT3 transcriptional activation and TNBC radioresistance. Finally, we demonstrated that TRIM32 and STAT3 phosphorylation are co-expressed in TNBC tissues. Moreover, high expression of TRIM32 and STAT3 phosphorylation is positively linked to poor prognosis of TNBC patients. Our study demonstrates that TRIM32 is a novel target for predicting radioresistance in TNBC patients.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据