Consequences of TRPV1 Knockout in Human U87 Glioblastoma Mediated by Capsaicin
JSHS · 2025
Overview
Glioblastoma is a highly aggressive brain malignancy with a 5 -year survival rate of 6.9%. The transient receptor potential vanilloid-1 (TRPV1) ion channel has been studied for its activation by capsaicin, a phytochemical with anti -cancer properties. TRPV1 knockout promotes tumor proliferation through p53 pathway inhibition, a crucial tumo r suppressor. While TRPV1 has been implicated in tumor suppression, the effects of its knockout on capsaicin -dosed glioblastoma remain unexplored. This study simulated TRPV1 knockout to elucidate the consequences of capsaicin on apoptosis, metastasis, and p53 expression in TRPV1 knockout U87 -MG glioblastoma. Using CRISPR-Cas9 technology, a TRPV1 knockout was simulated in human U87 glioblastoma. Knockout and control cells were treated with 100 -225 micromolar capsaicin and ethanol. WST-8 cell viability assays , scratch-healing migration, and RNA sequencing revealed that TRPV1 knockout amplifies capsaicin’s anti -tumor effects, effectively suppressing cancer. WST-8 cell viability assays, sampled at 24 h, 48 h, and 72 h, showed dose - and time-dependent apoptosis, with TRPV1 knockout cells exhibiting greater capsaicin -induced apoptosis. Scratch - healing migration assays at 24 h demonstrated that capsaicin-treated knockout cells exhibited no gap closure, while ethanol-treated knockout cells observed 100 micrometers of gap closure. RNA sequencing identified greater upregulation of p53 in knockout cells, suggesting increased apoptosis. IC50 values indicated that 164.4 micromolar capsaicin caused the most pronounced cancer suppressive effects on TRPV1 knockout cells. These findings imply that TRPV1 knockout enhances capsaicin’s anti -tumor effects, making TRPV1 a promising target in anti -cancer treatments. Applications of this research can explore the feasibility of capsaicin -based drugs to target TRPV1 in brain cancer patients.
Competition history
- JSHS 2025
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