ArticleCell communication and signaling : CCS2022
The Janus-faced role of TRPM2-S in retroperitoneal liposarcoma via increasing ROS levels.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Cancer Cell-Derived Large Extracellular Vesicles Promote Venous Thromboembolism by Activating NETosis Through Delivering CYBA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular feature-based classification of retroperitoneal liposarcoma: a prospective cohort study.eLife · 2025Observational
- The Combination of 5-FU and Resveratrol Can Suppress the Growth of Glioblastoma Cells Through Downregulation of TRPM2 and β-Catenin.Journal of molecular neuroscience : MN · 2024Article
- TRP Channels in Tumoral Processes Mediated by Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023Review
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8 authors.
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Abstract
backgroundRetroperitoneal liposarcoma (RPLS) is a specific soft tissue sarcoma with a high recurrence rate. The short isoform of transient receptor potential cation channel subfamily M member 2 (TRPM2-S) plays an important role in the regulation of reactive oxygen species (ROS). However, the association between TRPM2-S and RPLS and its underlying mechanisms remains unclear.
methodsThe expression of both TRPM2-S and TRPM2-L in RPLS tissues was verified by kimmunohistochemistry (IHC). The regulation on Ca
resultsThe IHC assays showed that TRPM2-S, but not TRPM2-L, was prognostic in RPLS. Low TRPM2-S level was associated with poor disease-free survival (DFS). Calcium influx signal intensity was significantly decreased under TRPM2-S overexpression, which resulted in a decrease in the levels of FOXO3a and PTEN. Correspondingly, the levels of pERK, pAKT, pP65, pGSK-3β, Bcl-2, and β-catenin were upregulated, and cellular ROS was gently increased under TRPM2-S overexpression. Moreover, TRPM2-S slightly promoted cell proliferation and inhibited apoptosis of RPLS cell lines under normoxia, but largely increased apoptosis rates under oxidative stress. The cleaved caspase3 was significantly upregulated by TRPM2-S overexpression under oxidative stress. N-Acetyl-L-cysteine (NAC), a small molecule antioxidant, could largely rescue RPLS cells from the apoptosis induced by H
conclusionTRPM2-S exerts Janus-faced effects in RPLS by increasing the ROS levels via inhibition on FOXO3a, which promotes cell proliferation under normoxia but induces apoptosis under oxidative stress. Video abstract.
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