ArticleFrontiers in pharmacology2026
CGRP remodels the acidic microenvironment and promotes pancreatic carcinoma progression by regulating NHE1 and CA9.
Article in Frontiers in pharmacology, 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
Introduction: Neurons can regulate cancer cells to modulate their survival and growth, the interplay between calcitonin gene-related peptide (CGRP) and the acidic tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDAC) remains unknown. Methods and Results: Here, we reported that CGRP expression and neuronal activation markers p-ERK/p-CREB were significantly elevated in PDAC tissues. Exogenous CGRP promoted PANC02 cell proliferation and migration, whereas CGRP knockout suppressed orthotopic tumor growth. Mechanistically, CGRP upregulated the proton transporters NHE1 and CA9, facilitating H Conclusion and Discussion: In conclusion, our findings uncover a functional connection between CGRPergic sensory neurons and the acidic TME, identifying the CGRP signaling pathway as a potential therapeutic target for PDAC. Despite these findings, the mechanistic conclusions remain correlative and require further validation, and the generalizability to human PDAC warrants future investigation.
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