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- W2896799163 abstract "Cyclin‐dependent kinase ( CDK ) 4 and CDK 6 inhibitors are effective therapeutic options for hormone receptor ( HR )‐positive, human epidermal growth factor receptor 2 ( HER 2)‐negative advanced breast cancer. Although CDK 4/6 inhibitors mainly target the cyclin D‐ CDK 4/6‐retinoblastoma tumor suppressor protein ( RB ) axis, little is known about the clinical impact of inhibiting phosphorylation of other CDK 4/6 target proteins. Here, we focused on other CDK 4/6 targets, SMAD proteins. We showed that a CDK 4/6 inhibitor palbociclib and activin‐ SMAD 2 signaling cooperatively inhibited cell cycle progression of a luminal‐type breast cancer cell line T47D. Palbociclib enhanced SMAD 2 binding to the genome by inhibiting CDK 4/6‐mediated linker phosphorylation of the SMAD 2 protein. We also showed that cyclin G2 plays essential roles in SMAD 2‐dependent cytostatic response. Moreover, comparison of the SMAD 2 Ch IP ‐seq data of T47D cells with those of Hs578T (triple‐negative breast cancer cells) indicated that palbociclib augmented different SMAD 2‐mediated functions based on cell type, and enhanced SMAD 2 binding to the target regions on the genome without affecting its binding pattern. In summary, palbociclib enhances the cytostatic effects of the activin‐ SMAD 2 signaling pathway, whereas it possibly strengthens the tumor‐promoting aspect in aggressive breast cancer." @default.
- W2896799163 created "2018-10-26" @default.
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- W2896799163 date "2018-11-16" @default.
- W2896799163 modified "2023-10-16" @default.
- W2896799163 title "Palbociclib enhances activin-SMAD-induced cytostasis in estrogen receptor-positive breast cancer" @default.
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- W2896799163 doi "https://doi.org/10.1111/cas.13841" @default.
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