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- W2767156586 abstract "Summary Cancer‐associated fibroblasts ( CAF s) in the tumor microenvironment have been associated with formation of a dynamic and optimized niche for tumor cells to grow and evade cell death induced by therapeutic agents. We recently reported that ablation of β‐catenin expression in stromal fibroblasts and CAF s disrupted their biological activities in in vitro studies and in an in vivo B16F10 mouse melanoma model. Here, we show that the development of a BRAF ‐activated PTEN ‐deficient mouse melanoma was significantly suppressed in vivo after blocking β‐catenin signaling in CAF s. Further analysis revealed that expression of phospho‐Erk1/2 and phospho‐Akt was greatly reduced, effectively abrogating the activating effects and abnormal cell cycle progression induced by Braf and Pten mutations. In addition, the epithelial–mesenchymal transition ( EMT )‐like process was also suppressed in melanoma cells. Taken together, our data highlight an important crosstalk between CAF s and the RAF ‐ MEK ‐ ERK signaling cascade in BRAF ‐activated melanoma and may offer a new approach to abrogate host‐dependent drug resistance in targeted therapy." @default.
- W2767156586 created "2017-11-10" @default.
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- W2767156586 date "2017-11-05" @default.
- W2767156586 modified "2023-10-11" @default.
- W2767156586 title "Suppression of MAPK signaling in BRAF-activated PTEN-deficient melanoma by blocking β-catenin signaling in cancer-associated fibroblasts" @default.
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- W2767156586 doi "https://doi.org/10.1111/pcmr.12657" @default.
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