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Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from in vitro and in vivo models

  • Authors:
    • Byung Jo Choi
    • Ho Joong Choi
    • Dosang Lee
    • Jung Hyun Park
    • Tae Ho Hong
    • Hee-Jung Jung
    • Ga-Hee Jo
    • Ok-Hee Kim
    • Say-June Kim

  • View Affiliations / Copyright

    Affiliations: Department of Surgery, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon 34943, Republic of Korea, Division of Hepatobiliary Pancreatic Surgery, Department of Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea, Catholic Central Laboratory of Surgery, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea, Translational Research Team, Surginex Co., Ltd., Seoul 06591, Republic of Korea
    Copyright: © Choi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 310
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    Published online on: September 5, 2025
       https://doi.org/10.3892/mmr.2025.13675
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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.
View Figures

Figure 1

In vitro anticancer effects of rupatadine on pancreatic cancer cell lines. (A) Chemical structure of rupatadine. As a cationic amphiphilic drug, the structure of rupatadine, comprising a hydrophobic ring and a cationic amine group, facilitates its penetration through the plasma membrane. (B) Dose-response curves comparing the effects of rupatadine on AsPC-1 and MIA-PaCa-2 pancreatic cancer cells with those on HPSC (bottom). For the cancer cell lines, a dose-dependent decrease in viability is observed with rupatadine concentrations from 0 to 50 µM, with IC50 values of 23.5 µM (24 h) and 24.9 µM (48 h) for AsPC-1 cells (top, left) and 30.9 µM (24 h) and 35.1 µM (48 h) for MIA-PaCa-2 cells (top, right). By contrast, HPSCs (bottom) exhibit significantly higher IC50 values of 66.8 µM (24 h) and 132.0 µM (48 h), indicating lower sensitivity to rupatadine. (C) Induction of apoptosis in AsPC-1 cells. Western blot analysis shows a dose-dependent increase in the levels of pro-apoptotic markers PARP and cleaved caspase-3 and a reduction in the anti-apoptotic marker Mcl-1 in AsPC-1 pancreatic cancer cells following treatment with rupatadine, ranging from 0 to 25 µM (P<0.05). (D) Induction of apoptosis in MIA-PACA-2 cells. MIA-PACA-2 cells treated with rupatadine showed increased pro-apoptotic markers and decreased anti-apoptotic markers, similar to AsPC-1 cells, indicating rupatadine's consistent pro-apoptotic effect (P<0.05). Relative densities of individual markers had been quantified using Image J software and then were normalized to that of β-actin in each group. Values are presented as mean ± SD of three independent experiments. *P<0.05 vs. the control after 24 h; +P<0.05 vs. the control after 48 h. HPSC, human pancreatic stellate cells; Mcl-1, Myeloid cell leukemia-1; c-, cleaved; cas3, caspase 3.

Figure 2

Effects of rupatadine on TGF-β signaling and EMT marker regulation. (A) In AsPC-1 pancreatic cancer cells, rupatadine exhibits a dose-dependent decrease in TGF-βRI expression and reduces the ratio of p-SMAD2/3 to total SMAD2/3, suggesting an inhibition of the TGFβ1 pathway. (B) In MIA PaCa-2 cells, analogous dose-dependent effects of rupatadine are observed, consistent with findings in AsPC-1 cells, further validating the drug's role in modulating TGF-β signaling and EMT. Relative densities of individual markers had been quantified using Image J software and then were normalized to that of β-actin in each group. Values are presented as mean ± SD of three independent experiments. *P<0.05 vs. the control. EMT, epithelial-mesenchymal transition; TGF-βRI, transforming growth factor β receptor type I; p-, phosphorylated; N-cad, N-cadherin; E-cad, E-cadherin.

Figure 3

Impact of rupatadine on the migration of pancreatic cancer cells. (A) Wound healing assay in AsPC-1 cells. The assay involved monitoring wound closure in a monolayer of AsPC-1 cells, scratched and then treated with varying concentrations of rupatadine (0.01–25 µM). Results showed that higher concentrations of rupatadine significantly expanded the scratch area, indicating reduced cell migration. (B) Wound healing assay in MIA PaCa2 cells. Similar patterns to AsPC-1 cells were observed. Values are presented as mean ± SD of three independent experiments. Scale bar, 200 µm. *P<0.05 vs. the control.

Figure 4

Immunofluorescence assay showing rupatadine's influence on EMT in pancreatic cancer cells. (A) Immunofluorescence in AsPC-1 cells. The assay revealed a dose-dependent increase in E-cadherin immunofluorescence and a decrease in Snail and Vimentin, indicative of EMT inhibition. (B) Immunofluorescence in MIA PaCa-2 cells. Similar patterns to AsPC-1 cells were observed. Values are presented as mean ± SD of three independent experiments. Percentages of immunoreactive areas were measured using NIH Image J and expressed as relative values to those in control tissues. Scale bar, 150 µm. *P<0.05 vs. the control. EMT, epithelial-mesenchymal transition; E-cad; E-cadherin; Ct, control.

Figure 5

Anticancer efficacy of rupatadine in a pancreatic cancer xenograft mouse model. (A) Representative images of excised tumors from the control and rupatadine-treated groups on day 21 after initial treatment. (B) Tumor growth curve (top) showing a significantly slower tumor growth rate in the rupatadine-treated group compared to the control group. Body weight changes (bottom) indicate no significant differences between the groups, suggesting no systemic toxicity. (C) Tumor weight analysis on day 21 post-treatment, showing a significant reduction in the rupatadine-treated group (P<0.05). (D) TUNEL assay demonstrating a higher apoptosis index in the rupatadine-treated tumors compared to the control group (P<0.05). Scale bar, 150 µm (E) Western blot analysis of EMT and apoptosis-related markers in excised tumors. Rupatadine treatment increased E-cadherin and pro-apoptotic markers (PARP, PUMA) while reducing vimentin and the anti-apoptotic marker Mcl-1 (P<0.05). Relative densities of individual markers had been quantified using Image J software and then were normalized to that of β-actin in each group. Values are presented as mean ± SD of three independent experiments. *P<0.05 vs. the control. EMT, epithelial-mesenchymal transition; Mcl-1, Myeloid cell leukemia-1; E-cad; E-cadherin; Ct, control; PUMA, p53 upregulated modulator of apoptosis.

Figure 6

Impact of rupatadine on histological changes in a pancreatic cancer xenograft mouse model. (A) H&E staining of excised tumor tissues, demonstrating a notable reduction in tumor cell density in the rupatadine-treated group. (B) Immunohistochemical analysis for the markers of apoptosis and EMT. Rupatadine-treated group exhibited increased immunoreactivity for the pro-apoptotic marker BIM and decreased expression of the anti-apoptotic marker Mcl-1. In addition, the rupatadine-treated group exhibited decreased immunoreactivity for the epithelial marker E-cadherin and decreased expression of the mesenchymal marker Snail. For 10× magnification, the scale bar is 100 µm; for 20× magnification, the scale bar is 50 µm. (C) Pharmacokinetic and tissue distribution analysis of rupatadine in vivo. (Left) Plasma concentration-time curve of rupatadine following intravenous administration (10 mg/kg) in mice. Rupatadine was rapidly cleared from plasma, with undetectable levels beyond 180 min. (Right) Tissue distribution of rupatadine at 5 and 60 min post-injection, showing predominant accumulation in the liver and kidneys at early time points, with minimal retention after 60 min. Values are presented as mean ± SD of three independent experiments. Percentages of immunoreactive areas were measured using Image J (National Institute of Health) and expressed as relative values to those in control tissues. *P<0.05 vs. the control. H&E, hematoxylin and eosin staining; EMT, epithelial-mesenchymal transition; BIM, Bcl-2 interacting mediator of cell death; Ct, control; Mcl-1, Myeloid cell leukemia-1; E-cad, E-cadherin; Rupa, Rupatadine.
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Copy and paste a formatted citation
Spandidos Publications style
Choi BJ, Choi HJ, Lee D, Park JH, Hong TH, Jung H, Jo G, Kim O and Kim S: Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models. Mol Med Rep 32: 310, 2025.
APA
Choi, B.J., Choi, H.J., Lee, D., Park, J.H., Hong, T.H., Jung, H. ... Kim, S. (2025). Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models. Molecular Medicine Reports, 32, 310. https://doi.org/10.3892/mmr.2025.13675
MLA
Choi, B. J., Choi, H. J., Lee, D., Park, J. H., Hong, T. H., Jung, H., Jo, G., Kim, O., Kim, S."Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models". Molecular Medicine Reports 32.5 (2025): 310.
Chicago
Choi, B. J., Choi, H. J., Lee, D., Park, J. H., Hong, T. H., Jung, H., Jo, G., Kim, O., Kim, S."Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models". Molecular Medicine Reports 32, no. 5 (2025): 310. https://doi.org/10.3892/mmr.2025.13675
Copy and paste a formatted citation
x
Spandidos Publications style
Choi BJ, Choi HJ, Lee D, Park JH, Hong TH, Jung H, Jo G, Kim O and Kim S: Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models. Mol Med Rep 32: 310, 2025.
APA
Choi, B.J., Choi, H.J., Lee, D., Park, J.H., Hong, T.H., Jung, H. ... Kim, S. (2025). Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models. Molecular Medicine Reports, 32, 310. https://doi.org/10.3892/mmr.2025.13675
MLA
Choi, B. J., Choi, H. J., Lee, D., Park, J. H., Hong, T. H., Jung, H., Jo, G., Kim, O., Kim, S."Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models". Molecular Medicine Reports 32.5 (2025): 310.
Chicago
Choi, B. J., Choi, H. J., Lee, D., Park, J. H., Hong, T. H., Jung, H., Jo, G., Kim, O., Kim, S."Rupatadine suppresses tumor growth and EMT in pancreatic cancer: Evidence from <em>in vitro</em> and <em>in vivo</em> models". Molecular Medicine Reports 32, no. 5 (2025): 310. https://doi.org/10.3892/mmr.2025.13675
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