自噬
转移
癌症研究
生物
乳腺癌
基因敲除
恶性肿瘤
体内
转录因子
细胞迁移
转移性乳腺癌
细胞生长
下调和上调
癌症
细胞
细胞凋亡
生物化学
遗传学
生物技术
基因
作者
Heng Xiao,Jing Long,Xiang Chen,Miduo Tan
标识
DOI:10.1016/j.yexcr.2022.113234
摘要
Recurrence and metastasis affect the survival rate of breast cancer patients. The fundamental reason lies in the lack of understanding of the mechanism of breast cancer metastasis. In this study, the proliferation, migration and invasion abilities of breast cancer cells were evaluated. The mechanism of NUPR1/TFE3 signaling pathway on autophagy-related proteins and migration-invasion-related proteins was examined in cell model in vitro. The effects of NUPR1 on malignancy formation and metastasis were investigated in vivo. We found that NUPR1 was upregulated in breast cancer cells and tissues. NUPR1 knockdown inhibited the proliferation, migration and invasion of ZR-75-30 cells and inhibited malignancy formation and metastasis in vivo. Mechanically, NUPR1 promoted autophagy by activating of TFE3 transcription, thereby regulating breast cancer metastasis. This paper indicates that NUPR1 activates autophagy through the TFE3 signaling pathway to promote breast cancer metastasis, and provides a biological basis for the intervention of blocking distant metastasis.
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