80P Dual cell cycle arrest in KRAS mutant cell lines by co-inhibition of MAPK and Hippo-YAP1 pathways

Abstract

The Kirsten rat sarcoma viral oncogene homolog (KRAS) belongs to the Ras protein family of small Guanosine-Triphosphate hydrolases (GTPases) that favors the activation of the mitogen-activated protein kinases (MAPK) pathway involved in cell survival and proliferation. KRAS mutations (mutKRAS) can initiate and maintain cancer progression, they are present in solid tumors (lung, colon and pancreas) and treatments remain difficult. The transcriptional co-activator (YAP1) and the transcription factor family Transcriptional enhanced associate domain 1-4 (TEAD1-4) are downstream effectors of the Hippo-YAP1 pathway that regulates cell proliferation, cell survival and cell migration.