Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from in vitro and in vivo models
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- Published online on: September 5, 2025 https://doi.org/10.3892/mmr.2025.13675
- Article Number: 310
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Copyright: © Choi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Rupatadine, primarily used for treating allergic rhinitis as a selective histamine H1 receptor and platelet‑activating factor antagonist, has potential anticancer properties, specifically through inducing lysosomal membrane permeabilization. The present study explores the efficacy of rupatadine in pancreatic cancer. The study assessed the effects of rupatadine on cell viability in AsPC‑1 and MIA PaCa‑2 pancreatic cancer cell lines at concentrations ranging from 0.001 to 50 µM. Additionally, a xenograft pancreatic cancer model in mice was used, with rupatadine administered intraperitoneally at 3 mg/kg three times weekly for 3 weeks. Tumor weights were measured 21 days post‑treatment. Western blot analysis and immunohistochemical staining were conducted on excised tumor tissues to evaluate the impact on EMT and apoptosis. Rupatadine exhibited a concentration‑dependent decrease in cell viability in both pancreatic cancer cell lines (P<0.05). In vivo, rupatadine significantly reduced tumor weight in the xenograft model compared with control groups (P<0.05). Further analysis revealed inhibition of EMT, evidenced by increased E‑cadherin and decreased Vimentin and Snail levels. Apoptosis was enhanced, as shown by increased PARP and decreased Mcl‑1 levels (P<0.05). Rupatadine shows significant anticancer potential in pancreatic cancer by inhibiting EMT and promoting apoptosis. These findings suggest that rupatadine could be developed as a novel therapeutic agent for pancreatic cancer, meriting further clinical investigation.
