Regulation of tamoxifen sensitivity by the PLAC8/MAPK pathway axis is antagonized by curcumin-induced protein stability change.
Misha MaoDengdi HuJingjing YangYongxia ChenXun ZhangJianguo ShenRongyue TengJichun ZhouLinbo WangPublished in: Journal of molecular medicine (Berlin, Germany) (2021)
Tamoxifen resistance remains the major obstacle to the estrogen receptor positive breast cancer endocrine therapy. Placenta-specific 8 (PLAC8) has been implicated in epithelial-mesenchymal transition and tumorigenesis. However, the molecular mechanisms underlying PLAC8 function in the context of tamoxifen resistance are unclear. Curcumin has attracted considerable attention in the last decades. It is isolated from Curcuma longa and has beneficial effects in cancer therapy. We studied this property by using MCF-7 and tamoxifen-resistant breast cancer cells (MCF-7/TAM) cell lines. PLAC8 can regulate MCF-7/TAM cell drug sensitivity through the MAPK/ERK pathway and shows the potential effects of curcumin or as a possible druggable target against tamoxifen failure.
Keyphrases
- breast cancer cells
- estrogen receptor
- positive breast cancer
- signaling pathway
- epithelial mesenchymal transition
- cancer therapy
- pi k akt
- oxidative stress
- single cell
- emergency department
- stem cells
- cell proliferation
- working memory
- cell therapy
- drug induced
- mesenchymal stem cells
- small molecule
- bone marrow
- risk assessment
- electronic health record
- replacement therapy