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The Janus-faced role of TRPM2-S in retroperitoneal liposarcoma via increasing ROS levels

Xiangji Li1,2, Fanqin Bu2, Shixiang Ma1

  • 1Department of Retroperitoneal Tumor Surgery, Peking University International Hospital, Peking University Eighth School of Clinical Medicine, Beijing, 102206, People's Republic of China.

Cell Communication and Signaling : CCS
|August 25, 2022
PubMed
Abstract

Insights

The short isoform of transient receptor potential cation channel subfamily M member 2 (TRPM2-S) has dual effects in retroperitoneal liposarcoma (RPLS). It promotes proliferation under normal conditions but induces apoptosis under oxidative stress by increasing reactive oxygen species (ROS).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Retroperitoneal liposarcoma (RPLS) is a soft tissue sarcoma with a high recurrence rate.
  • The short isoform of transient receptor potential cation channel subfamily M member 2 (TRPM2-S) is involved in reactive oxygen species (ROS) regulation.
  • The specific role and mechanisms of TRPM2-S in RPLS remain largely unknown.

Purpose of the Study:

  • To investigate the association between TRPM2-S and RPLS.
  • To elucidate the underlying molecular mechanisms of TRPM2-S in RPLS.
  • To determine the prognostic value of TRPM2-S in RPLS patients.

Main Methods:

  • Immunohistochemistry (IHC) to assess TRPM2-S and TRPM2-L expression in RPLS tissues.
  • Fluo-4 AM staining to evaluate TRPM2-S-mediated calcium influx.
  • EdU staining and flow cytometry for cell proliferation and apoptosis assays, respectively.
  • DCFH-DA probe for cellular ROS assessment.
  • Western blotting to explore underlying molecular pathways.

Main Results:

  • TRPM2-S expression, not TRPM2-L, was prognostic in RPLS, with low TRPM2-S associated with poor disease-free survival.
  • TRPM2-S overexpression decreased calcium influx, leading to reduced FOXO3a and PTEN levels, and increased pERK, pAKT, pP65, pGSK-3β, Bcl-2, and β-catenin.
  • TRPM2-S promoted RPLS cell proliferation and inhibited apoptosis under normoxia, but significantly increased apoptosis under oxidative stress, evidenced by elevated cleaved caspase-3.

Conclusions:

  • TRPM2-S exhibits dual roles in RPLS, promoting proliferation under normoxia and inducing apoptosis under oxidative stress.
  • TRPM2-S increases ROS levels by inhibiting FOXO3a, contributing to its context-dependent effects on RPLS cells.
  • TRPM2-S represents a potential therapeutic target, with its effects modulated by the cellular oxidative stress environment.
Keywords:
Dual effectsPrognosisROSRetroperitoneal liposarcomaTRPM2-S

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