ArticleInternational journal of biological macromolecules2026
Loss of TRPV1 may shift capsaicin response from MAPK-CASC11-MYC protection to mitochondrial apoptosis in glioblastoma U87 cells.
Article in International journal of biological macromolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Glioblastoma multiforme is an aggressive and therapy-resistant tumor, necessitating the identification of novel therapeutic targets. Here, we investigated the role of transient receptor potential vanilloid 1 (TRPV1) in mediating capsaicin-induced changes in cell viability in U87 glioblastoma cells. Wild-type cells tolerated capsaicin concentrations up to 175 μM, whereas TRPV1 knockout (TRPV1KO) cells exhibited reduced viability at 164 μM, indicating a cytoprotective function of TRPV1. Transcriptomic analyses revealed that wild-type cells activated the MAPK-MSTRG.66879-MYC-HSF1-axis, resulting in robust induction of heat shock proteins (HSPA1B, HSPA6, HSP90AA1) and dual-specificity phosphatases (DUSP1, DUSP8, DUSP10), which collectively maintained protein homeostasis and mitigated cellular damage. In contrast, TRPV1KO cells displayed impaired calcium-mediated MAPK activation, leading to altered mitochondrial oxidative phosphorylation, significant changes in electron transport chain (ETC I, II, III, IV), and enhanced intrinsic apoptosis through HRK. Notably, two long non-coding RNAs, MSTRG.56099 and MSTRG.66879, were identified as potential cis-regulators of DUSP1 and MYC, respectively. MSTRG.66879, upregulated in wild-type cells, appeared to form a TRPV1-associated regulatory axis with MYC and miR-182, promoting cell survival under capsaicin exposure. Disruption of this network in TRPV1KO cells sensitized them to capsaicin-induced apoptosis. Collectively, TRPV1 orchestrates calcium influx, MAPK signaling, heat shock protein induction, and noncoding RNA-mediated regulation to facilitate glioblastoma cell adaptation, suggesting that targeting TRPV1 and the MSTRG.66879-MYC axis may offer new therapeutic avenues and biomarkers for glioblastoma management.
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