Open AccessTumors driven by RAS signaling harbor a natural vulnerability to oncolytic virus M1
Author(s) -
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
Publication year - 2020
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1002/1878-0261.12820
Subject(s) - oncolytic virus , biology , cancer research , cancer cell , virotherapy , transcriptome , rna interference , cancer , gene , rna , genetics , gene expression , tumor cells
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 the effect of M1, while overexpression of p21 inhibits it. Inhibition of CDK2 by K03861 attenuates the efficacy of M1.