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Molecular Cancer Research
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Cancer Genes and Networks

Suppression of MET Signaling Mediated by Pitavastatin and Capmatinib Inhibits Oral and Esophageal Cancer Cell Growth

Bo Xu, Tomoki Muramatsu and Johji Inazawa
Bo Xu
1Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
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Tomoki Muramatsu
1Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
2Laboratory for Integrated Research Projects on Intractable Diseases, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
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  • For correspondence: johinaz.cgen@mri.tmd.ac.jp muracgen@tmd.ac.jp
Johji Inazawa
1Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
3Bioresource Research Center, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
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  • For correspondence: johinaz.cgen@mri.tmd.ac.jp muracgen@tmd.ac.jp
DOI: 10.1158/1541-7786.MCR-20-0688
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Abstract

Despite increasing knowledge on oral and esophageal squamous cell carcinoma (OSCC and ESCC), specific medicines against both have not yet been developed. Here, we aimed to find novel anticancer drugs through functional cell-based screening of an FDA-approved drug library against OSCC and ESCC. Pitavastatin, an HMGCR inhibitor, emerged as an anticancer drug that inhibits tumor growth by downregulating AKT and ERK signals in OSCC and ESCC cells. One of the mechanisms by which pitavastatin inhibits cell growth might be the suppression of MET signaling through immature MET due to dysfunction of the Golgi apparatus. Moreover, the sensitivity of tumor growth to pitavastatin might be correlated with GGPS1 expression levels. In vivo therapeutic models revealed that the combination of pitavastatin with capmatinib, a MET-specific inhibitor, dramatically reduced tumor growth. Our findings suggest that GGPS1 expression could be a biomarker in cancer therapy with pitavastatin, and the combination of pitavastatin with capmatinib might be a promising therapeutic strategy in OSCC and ESCC.

Implications: This study provides new insight into the mechanism of pitavastatin as an anticancer drug and suggests that the combination of pitavastatin with capmatinib is a useful therapeutic strategy in OSCC and ESCC.

Footnotes

  • Note: Supplementary data for this article are available at Molecular Cancer Research Online (http://mcr.aacrjournals.org/).

  • Mol Cancer Res 2021;XX:XX–XX

  • Received August 6, 2020.
  • Revision received October 9, 2020.
  • Accepted December 9, 2020.
  • Published first December 22, 2020.
  • ©2020 American Association for Cancer Research.

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This OnlineFirst version was published on January 29, 2021
doi: 10.1158/1541-7786.MCR-20-0688

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Suppression of MET Signaling Mediated by Pitavastatin and Capmatinib Inhibits Oral and Esophageal Cancer Cell Growth
Bo Xu, Tomoki Muramatsu and Johji Inazawa
Mol Cancer Res January 29 2021 DOI: 10.1158/1541-7786.MCR-20-0688

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Suppression of MET Signaling Mediated by Pitavastatin and Capmatinib Inhibits Oral and Esophageal Cancer Cell Growth
Bo Xu, Tomoki Muramatsu and Johji Inazawa
Mol Cancer Res January 29 2021 DOI: 10.1158/1541-7786.MCR-20-0688
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Molecular Cancer Research
eISSN: 1557-3125
ISSN: 1541-7786

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