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• W2335232153 abstract "Why are YAP1 and c-Myc often overexpressed (or activated) in KRAS-driven cancers and drug resistance? Here, we propose that there are two independent pathways in tumor proliferation: one includes MAPK/ERK and PI3K/A kt/mTOR; and the other consists of pathways leading to the expression (or activation) of YAP1 and c-Myc. KRAS contributes through the first. MYC is regulated by e.g. β-catenin, Notch and Hedgehog. We propose that YAP1 and ERK accomplish similar roles in cell cycle control, as do β-catenin and PI3K. This point is compelling, since the question of how YAP1 rescues K-Ras or B-Raf ablation has recently captured much attention, as well as the mechanism of resistance to PI3K inhibitors. The similarity in cell cycle actions of β-catenin and PI3K can also clarify the increased aggressiveness of lung cancer when both K-Ras and β-catenin operate. Thus, we propose that the two pathways can substitute one another – or together amplify each other – in promoting proliferation. This new understanding of the independence and correspondence of the two pathways in cancer – MAPK/ERK and PI3K/Akt/mTOR; and YAP1 and c-Myc – provide a coherent and significant picture of signaling-driven oncogenic proliferation and may help in judicious, pathway-based drug discovery." @default.
• W2335232153 created "2016-06-24" @default.
• W2335232153 creator A5011513198 @default.
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• W2335232153 date "2016-10-01" @default.
• W2335232153 modified "2023-10-17" @default.
• W2335232153 title "Oncogenic KRAS signaling and YAP1/β-catenin: Similar cell cycle control in tumor initiation" @default.
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• W2335232153 doi "https://doi.org/10.1016/j.semcdb.2016.04.001" @default.
• W2335232153 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27058752" @default.
• W2335232153 hasPublicationYear "2016" @default.
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