ArticleCellular oncology (Dordrecht, Netherlands)2024
Targeting CA9 restricts pancreatic cancer progression through pH regulation and ROS production.
Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Lung adenocarcinoma cells respond differently to mechanical stress in 3D versus 2D environments.Communications biology · 2025Article
- UBC4: A Repurposed Drug Regimen for Adjunctive Use During Bladder Cancer Treatment.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
purposeLactate is a key metabolite produced by glycolytic metabolism, yet it also serves as an energy source for cancer cells. Lactate accumulation in the tumor microenvironment (TME) has been demonstrated to correlate with immunosuppressive TME and tumor progression. As a highly glycolytic tumor, it is crucial to decipher the underlying mechanism in pancreatic ductal adenocarcinoma (PDAC).
methodsBioinformation analysis was used to identify lactate mediated carbonic anhydrase IX (CA9) upregulation. CCK-8, colony formation and mouse xenograft assay were utilized to study the effect of CA9 in PDAC. ECAR, OCR and pHi measurement confirmed the impacts of CA9 in Warburg phenotype. Using confocal microscopy, flow cytometry, qRT-PCR, co-IP, we validated the signaling pathways in PDAC to regulate reactive oxygen species (ROS) production.
resultsWe confirmed that CA9 is highly expressed in PDAC and positively regulated by lactate levels. CA9 can enhance the proliferative and migratory capabilities of PDAC cells. Pharmacologic inhibition or knockdown of CA9 significantly reduce pHi, increase the intracellular lactate and reverse the Warburg phenotype. The intracellular lactate accumulation caused by CA9 knockdown upregulates ROS and mitochondrial dysfunction. Furthermore, it was discovered that the competitive binding of CA9 with FUS inhibits the facilitation of FUS on NOX4 pre-mRNA splicing.
conclusionCollectively, our data illustrate that CA9 has a direct regulatory role in pHi homeostasis and ROS production, providing a potential therapeutic target for PDAC treatment.
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