ArticleNeuro-oncology advances
Repurposing salmon calcitonin for glioblastoma treatment: Targeting Yes-associated Protein (YAP)/ Transcriptional co‑activator with PDZ‑binding motif (TAZ) via hippo pathway activation.
Article in Neuro-oncology advances. 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
Background: Glioblastoma (GBM) remains a deadly brain tumor. Activation of the wild-type calcitonin receptor (CTR) by salmon calcitonin (sCT) suppresses glioma growth, whereas patient-derived CTR mutants drive tumor progression and correlate with poor survival. This study delineates the mechanisms underlying sCT-mediated tumor suppression and reveals structural defects in oncogenic CTR variants. Methods: Proteome analysis of sCT-treated glioma cells was done to dissect the altered signaling. Multiple experimental approaches were used to elucidate the signaling behind CTR-dependent Hippo pathway activation. The therapeutic efficacy of sCT on the growth of human/murine glioma stem-like cells (GSC)-initiated tumors in an orthotopic mouse glioma model was assessed. Extensive microsecond-scale all-atom molecular dynamics simulations were performed to elucidate the structural impairments in CTR mutants. Results: sCT treatment activated Hippo signaling as demonstrated by enhanced phosphorylation and subsequent degradation of YAP/TAZ and suppressed glioma growth through cAMP/PKA/LATS1 signaling in vitro. However, GSCs expressing a phosphorylation-resistant YAP mutant were refractory to sCT treatment Conclusions: We establish that activation of the sCT-CTR axis suppresses glioma growth by inhibiting YAP/TAZ through Hippo pathway activation. We further delineate the structural aberrations responsible for the functional loss in patient-derived CTR mutants. Thus, we present compelling evidence supporting the therapeutic repurposing of calcitonin for GBM treatment.
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