ArticleFrontiers in pharmacology2024
Terfenadine, a histamine H1 receptor antagonist, induces apoptosis by suppressing STAT3 signaling in human colorectal cancer HCT116 cells.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting histamine signaling: repurposing antihistamines for cancer chemotherapy and immunotherapy.Archives of pharmacal research · 2026Review
- Inhibition of RBM23 induces ferroptosis in colon cancer cells via c-Myc regulation.Cancer cell international · 2026Article
- Antihistamine drug terfenadine suppressed the cycle progression of gastric cancer cells by targeting PI3K/AKT/mTOR signaling.Frontiers in pharmacology · 2026Article
- A high-throughput screening approach to discover potential colorectal cancer chemotherapeutics: repurposing drugs to identify novel disruptors of 14-3-3 proteins.Cell death & disease · 2025Article
- Domperidone Induces Apoptosis through Suppression of STAT3 Signaling in Human Renal Cancer Caki-2 Cells.Journal of cancer prevention · 2025Article
- Machine learning model reveals the risk, prognosis, and drug response of histamine-related signatures in pancreatic cancer.Discover oncology · 2025Article
- Repurposing terfenadine and domperidone for inhibition of apoptotic gene association in colorectal cancer: A system pharmacology approach integrated with molecular docking, MD simulations, and post-MD simulation analysis.Bioinformatics and biology insights · 2025Article
- Review
- Pan-Cancer Insights: A Study of Microbial Metabolite Receptors in Malignancy Dynamics.Cancers · 2024Article
- Zinc finger protein 263 promotes colorectal cancer cell progression by activating STAT3 and enhancing chemoradiotherapy resistance.Scientific reports · 2024Article
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3 authors.
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Abstract
Introduction: Colorectal cancer is a highly aggressive and metastatic cancer with inadequate clinical outcomes. Given the crucial role of histamine and histamine receptors in colorectal carcinogenesis, this study aimed at exploring the anticancer effects of terfenadine against colorectal cancer HCT116 cells and elucidate its underlying mechanism. Methods: Herein, we examined the effect of terfenadine on growth and proliferation of HCT116 cells Results: Terfenadine markedly attenuated the viability of HCT116 cells by abrogating histamine H1 receptor (H1R) signaling. In addition, terfenadine modulated the balance of Bax and Bcl-2, triggering cytochrome c discharge in the cytoplasm, thereby stimulating the caspase cascade and poly-(ADP-ribose) polymerase (PARP) degradation. Moreover, terfenadine suppressed murine double minute-2 (Mdm2) expression, whereas p53 expression increased. Terfenadine suppressed STAT3 phosphorylation and expression of its gene products by inhibiting MEK/ERK and JAK2 activation in HCT116 cells. Furthermore, treatment with U0126, a MEK inhibitor, and AG490, a JAK2 inhibitor, dramatically diminished the phosphorylations of ERK1/2 and JAK2, respectively, leading to STAT3 downregulation. Likewise, terfenadine diminished the complex formation of MEK1/2 with β-arrestin 2. In addition, terfenadine dwindled the phosphorylation of PKC substrates. Terfenadine administration (10 mg/kg) substantially retarded the growth of HCT116 tumor xenografts Conclusion: Terfenadine induces the apoptosis of HCT116 cells by abrogating STAT3 signaling. Overall, this study supports terfenadine as a prominent anticancer therapy for colorectal cancer.
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