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CENPH Inhibits Rapamycin Sensitivity by Regulating GOLPH3-dependent mTOR Signaling Pathway in Colorectal Cancer.

Wei Wu1, Fan Wu1, Zaozao Wang1

  • 1Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Gastrointestinal Surgery IV, Peking University Cancer Hospital & Institute, Beijing 100142, China.

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Summary

Centromere protein H (CENPH) inhibits rapamycin sensitivity in colorectal cancer (CRC) by regulating the GOLPH3-dependent mTOR pathway. High CENPH expression indicates a better prognosis for CRC patients, suggesting its potential as a therapeutic target.

Keywords:
CENPHColorectal cancer (CRC)GOLPH3Prognosis.RapamycinmTOR

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Centromere protein H (CENPH) is a key component of active centromeres, with overexpression linked to poor prognosis in solid tumors.
  • Rapamycin, an mTOR inhibitor, exhibits antitumor activity and prevents intestinal tumorigenesis.
  • The prognostic significance of CENPH in colorectal cancer (CRC) and its influence on rapamycin sensitivity were previously unknown.

Purpose of the Study:

  • To investigate the prognostic value of CENPH in colorectal cancer (CRC).
  • To determine the role of CENPH in modulating sensitivity to rapamycin treatment.
  • To elucidate the underlying molecular mechanisms of CENPH's function in CRC.

Main Methods:

  • Cellular assays (MTT, colony formation) assessed CENPH's impact on CRC proliferation and rapamycin response.
  • Co-immunoprecipitation, GST pull-down, His-tag pull-down, and confocal microscopy analyzed CENPH-GOLPH3 interaction.
  • Western blot evaluated mTOR signaling pathway kinases.
  • Public CRC datasets analyzed clinical significance of CENPH expression.

Main Results:

  • CENPH inhibited CRC malignant phenotypes and reduced sensitivity to rapamycin.
  • CENPH attenuated mTORC1 and mTORC2 signaling via interaction with GOLPH3.
  • Elevated CENPH levels were found in CRC tissues, decreasing with tumor stage.
  • High CENPH expression correlated with favorable patient survival.

Conclusions:

  • CENPH inhibits rapamycin sensitivity by regulating the GOLPH3-dependent mTOR pathway.
  • High CENPH expression is associated with a better prognosis in CRC patients.
  • CENPH shows potential as a predictive marker for rapamycin sensitivity and a therapeutic target in CRC.