Integrin β4 promotes DNA damage-related drug resistance in triple-negative breast cancer via TNFAIP2/IQGAP1/RAC1

Anti-tumor drug resistance is a challenge for human triple-negative breast cancer (TNBC) treatment. Our previous work demonstrated that TNFAIP2 activates RAC1 to promote TNBC cell proliferation and migration. However, the mechanism by which TNFAIP2 activates RAC1 is unknown. In this study, we found...

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Detalles Bibliográficos
Autores principales: Fang, Huan, Ren, Wenlong, Cui, Qiuxia, Liang, Huichun, Yang, Chuanyu, Liu, Wenjing, Wang, Xinye, Liu, Xue, Shi, Yujie, Feng, Jing, Chen, Ceshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2023
Materias:
Cancer Biology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10547475/
https://www.ncbi.nlm.nih.gov/pubmed/37787041
http://dx.doi.org/10.7554/eLife.88483
Descripción
Sumario:Anti-tumor drug resistance is a challenge for human triple-negative breast cancer (TNBC) treatment. Our previous work demonstrated that TNFAIP2 activates RAC1 to promote TNBC cell proliferation and migration. However, the mechanism by which TNFAIP2 activates RAC1 is unknown. In this study, we found that TNFAIP2 interacts with IQGAP1 and Integrin β4. Integrin β4 activates RAC1 through TNFAIP2 and IQGAP1 and confers DNA damage-related drug resistance in TNBC. These results indicate that the Integrin β4/TNFAIP2/IQGAP1/RAC1 axis provides potential therapeutic targets to overcome DNA damage-related drug resistance in TNBC.

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