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PGRMC1 promotes NSCLC stemness phenotypes by disrupting TRIM56-mediated ubiquitination of AHR

Anqi Guan1, Ziyu Dai2, Chen Jiang2

  • 1Department of Geriatrics, Xiangya Hospital, Central South University, Changsha 410008, China; Xiangya Lung Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|July 26, 2024
PubMed

Insights

Progesterone receptor membrane component 1 (PGRMC1) drives cancer stem cell (CSC) traits and chemoresistance in non-small cell lung cancer (NSCLC) by inhibiting AHR ubiquitination. This reveals a new therapeutic target for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer stem cells (CSCs) drive tumor chemoresistance and recurrence.
  • The aryl hydrocarbon receptor (AHR) is crucial for maintaining CSC properties.
  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality.

Purpose of the Study:

  • To elucidate the role of progesterone receptor membrane component 1 (PGRMC1) in regulating AHR and CSC phenotypes in NSCLC.
  • To investigate the interaction between PGRMC1, AHR, and E3 ligase TRIM56 in NSCLC.
  • To identify potential therapeutic targets for overcoming CSC-mediated chemoresistance in NSCLC.

Main Methods:

  • Analysis of clinical data and tissue microarrays from NSCLC patients.
  • In vitro and in vivo experiments assessing CSC phenotypes and chemotherapy resistance.
  • Mass spectrometry to identify protein interactions and E3 ligases.
  • Investigation of protein ubiquitination and interaction modulation.

Main Results:

  • Elevated PGRMC1 expression correlates with poorer prognosis in NSCLC patients.
  • PGRMC1 overexpression enhances CSC phenotypes and chemotherapy resistance.
  • PGRMC1 modulates AHR ubiquitination by inhibiting the interaction between AHR and TRIM56.
  • Specific interaction sites between PGRMC1 and AHR were identified.

Conclusions:

  • A novel regulatory axis involving PGRMC1, AHR, and TRIM56 is identified in NSCLC.
  • PGRMC1 promotes CSC characteristics and chemoresistance by interfering with AHR ubiquitination via TRIM56.
  • Targeting this PGRMC1-AHR-TRIM56 pathway offers a potential strategy for NSCLC treatment.
Keywords:
AHRNSCLCPGRMC1StemnessTRIM56Ubiquitylation

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