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CLMP is a tumor suppressor that determines all-trans retinoic acid response in colorectal cancer

Zhenzhen Wu1, Xuanxuan Zhang1, Yunhe An2

  • 1Key Laboratory of Epigenetic Regulation and Intervention, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.

Developmental Cell
|November 9, 2023
PubMed

Insights

CAR-like membrane protein (CLMP) deficiency accelerates colorectal cancer (CRC) growth and ATRA resistance. Restoring CLMP function or inhibiting CYP26A1 may enhance ATRA therapy for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • CAR-like membrane protein (CLMP) is linked to congenital short bowel syndrome.
  • CLMP's role in colorectal cancer (CRC) pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the function of CLMP in colorectal cancer.
  • To elucidate the molecular mechanisms underlying CLMP's role in CRC.
  • To explore CLMP's impact on therapeutic resistance.

Main Methods:

  • Analysis of CLMP mutation and expression in CRC patients.
  • Assessment of CLMP deficiency effects on CRC tumorigenesis and growth in mouse models (ApcMin/+, AOM/DSS, orthotopic).
  • Investigation of CLMP's interaction with beta-catenin and Wnt/beta-catenin signaling.
  • Evaluation of cytochrome P450 hydroxylase A1 (CYP26A1) regulation and its impact on all-trans retinoic acid (ATRA) resistance.

Main Results:

  • CLMP is rarely mutated but significantly decreased in CRC.
  • CLMP deficiency accelerates CRC tumorigenesis, growth, and resistance to ATRA.
  • CLMP recruits beta-catenin to the cell membrane, inactivating Wnt/beta-catenin signaling.
  • CLMP deficiency upregulates CYP26A1, leading to ATRA resistance.

Conclusions:

  • CLMP acts as a tumor suppressor in colorectal cancer.
  • CLMP inactivation promotes CRC growth and ATRA resistance via CYP26A1 upregulation.
  • Targeting CYP26A1 may enhance ATRA's therapeutic efficacy in CRC.
Keywords:
ATRACLMPCRCCYP26A1β-catenin

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