Tumors driven by RAS signaling harbor a natural vulnerability to oncolytic virus M1

RAS/RAF/MAPK/p‐ERK signaling promotes the replication and oncolytic effect of M1 virus via inhibiting P21 and subsequent suppression of Cyclin‐dependent kinase 2 (CDK2). Inhibition of RAS/RAF/MAPK/p‐ERK signaling by sorafenib or U0126 suppresses the oncolytic effect of M1. Knockout of p21 enhances t...

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Veröffentlicht in:	Molecular oncology 2020-12, Vol.14 (12), p.3153-3168
Hauptverfasser:	Cai, Jing, Lin, Kaiying, Cai, Wei, Lin, Yuan, Liu, Xincheng, Guo, Li, Zhang, Jifu, Xu, Wencang, Lin, Ziqing, Wong, Chun Wa, Sander, Max, Hu, Jun, Yan, Guangmei, Zhu, Wenbo, Liang, Jiankai
Format:	Artikel
Sprache:	eng
Schlagworte:	Animal models Animals Antitumor activity Antiviral Agents - pharmacology biomarker Biomarkers, Tumor - metabolism Butadienes - pharmacology cancer accurate therapy Caspase CDKN1A Cell Line Cell Line, Tumor Clinical trials Cyclin-dependent kinase 2 Cyclin-Dependent Kinase Inhibitor p21 - deficiency Cyclin-Dependent Kinase Inhibitor p21 - metabolism DNA microarrays Female Gene Expression Regulation, Viral - drug effects Gene set enrichment analysis Genomes Humans Hybridization Immune response Immunohistochemistry Interferon Kinases Laboratory animals Mice, Inbred BALB C Mice, Nude Multiplicity of infection Mutation Mutation - genetics Neoplasms - metabolism Neoplasms - pathology Neoplasms - virology Nitriles - pharmacology Oncolysis oncolytic virus Oncolytic Viruses - drug effects Oncolytic Viruses - genetics Oncolytic Viruses - physiology Protein arrays Public health RAS ras Proteins - metabolism Ribonucleic acid RNA RNA, Small Interfering - metabolism Signal Transduction - drug effects Tumor cells Tumors Up-Regulation - drug effects Up-Regulation - genetics Viral infections Virus Replication - drug effects Virus Replication - genetics Viruses
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