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Inhibition of the mevalonate pathway enhances cancer cell oncolysis mediated by M1 virus

Author

Listed:
  • Jiankai Liang

    (Sun Yat-sen University)

  • Li Guo

    (Sun Yat-sen University)

  • Kai Li

    (The Sixth Affiliated Hospital of Sun Yat-sen University)

  • Xiao Xiao

    (The Third Affiliated Hospital of Sun Yat-sen University)

  • Wenbo Zhu

    (Sun Yat-sen University)

  • Xiaoke Zheng

    (The First Affiliated Hospital of Sun Yat-sen University)

  • Jun Hu

    (Sun Yat-sen University)

  • Haipeng Zhang

    (Sun Yat-sen University)

  • Jing Cai

    (Sun Yat-sen University)

  • Yaya Yu

    (Sun Yat-sen University)

  • Yaqian Tan

    (Sun Yat-sen University)

  • Chuntao Li

    (Sun Yat-sen University)

  • Xincheng Liu

    (Sun Yat-sen University)

  • Cheng Hu

    (The Third Affiliated Hospital of Sun Yat-sen University)

  • Ying Liu

    (The Third Affiliated Hospital of Sun Yat-sen University)

  • Pengxin Qiu

    (Sun Yat-sen University)

  • Xingwen Su

    (Sun Yat-sen University)

  • Songmin He

    (Weill Cornell Medical College)

  • Yuan Lin

    (Sun Yat-sen University
    Sun Yat-sen University)

  • Guangmei Yan

    (Sun Yat-sen University)

Abstract

Oncolytic virus is an attractive anticancer agent that selectively lyses cancer through targeting cancer cells rather than normal cells. Although M1 virus is effective against several cancer types, certain cancer cells present low sensitivity to it. Here we identified that most of the components in the cholesterol biosynthesis pathway are downregulated after M1 virus infection. Further functional studies illustrate that mevalonate/protein farnesylation/ras homolog family member Q (RHOQ) axis inhibits M1 virus replication. Further transcriptome analysis shows that RHOQ knockdown obviously suppresses Rab GTPase and ATP-mediated membrane transporter system, which may mediate the antiviral effect of RHOQ. Based on this, inhibition of the above pathway significantly enhances the anticancer potency of M1 virus in vitro, in vivo, and ex vivo. Our research provides an intriguing strategy for the rational combination of M1 virus with farnesyl transferase inhibitors to enhance therapeutic efficacy.

Suggested Citation

  • Jiankai Liang & Li Guo & Kai Li & Xiao Xiao & Wenbo Zhu & Xiaoke Zheng & Jun Hu & Haipeng Zhang & Jing Cai & Yaya Yu & Yaqian Tan & Chuntao Li & Xincheng Liu & Cheng Hu & Ying Liu & Pengxin Qiu & Xing, 2018. "Inhibition of the mevalonate pathway enhances cancer cell oncolysis mediated by M1 virus," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03913-6
    DOI: 10.1038/s41467-018-03913-6
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    Cited by:

    1. Li Guo & Cheng Hu & Yang Liu & Xiaoyu Chen & Deli Song & Runling Shen & Zhanzhen Liu & Xudong Jia & Qinfen Zhang & Yuanzhu Gao & Zhezhi Deng & Tao Zuo & Jun Hu & Wenbo Zhu & Jing Cai & Guangmei Yan & , 2023. "Directed natural evolution generates a next-generation oncolytic virus with a high potency and safety profile," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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