ArticlePharmaceutical biology2020
Arecoline suppresses epithelial cell viability by upregulating tropomyosin-1 through the transforming growth factor-β/Smad pathway.
Article in Pharmaceutical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Tropomyosin-1 positively regulates TGF-β/Smad3 signaling through STUB1 in arecoline-induced oral submucosal fibrosis.Odontology · 2026Article
- Curcumin suppresses EMT to alleviate oral submucous fibrosis progression through XIST/miR-25-3p-mediated inactivation of the TGF-β1/Smads signalling pathway.International dental journal · 2026Article
- Oral submucous fibrosis: pathogenesis and therapeutic approaches.International journal of oral science · 2025Review
- Overlap in oncogenic and pro-inflammatory pathways associated with areca nut and nicotine exposure.Cancer pathogenesis and therapy · 2024Article
- Identification of a BRAF/PA28γ/MEK1 signaling axis and its role in epithelial-mesenchymal transition in oral submucous fibrosis.Cell death & disease · 2022Article
- Knockdown of LncRNA NEAT1 inhibits myofibroblast activity in oral submucous fibrosis through miR-760/TPM1 axis.Journal of dental sciences · 2022Article
- Circular CDC like kinase 1 suppresses cell apoptosis through miR-18b-5p/Y-box protein 2 axis in oral squamous cell carcinoma.Bioengineered · 2022Article
- Arecae pericarpium extract induces porcine lower-esophageal-sphincter contraction via muscarinic receptors.BMC complementary medicine and therapies · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextOral submucous fibrosis (OSF) is a chronic and progressive disease. Arecoline, present in betel nuts, has been proposed as a vital aetiological factor. However, the underlying mechanism remains unclear.
objectivesThis research elucidates the expression of tropomyosin-1 (TPM1) and its regulation mechanism in HaCaT cells treated with arecoline. MATERIALS AND
methodsHaCaT cells were assigned into three groups: (1) Control; (2) Treated with arecoline (0.16 mM) for 48 h (3) Treated with arecoline (0.16 mM) and transfected with small interfering RNA (siRNA) for TPM1 (50 nM) for 48 h. CCK8, cell cycle, and apoptosis phenotypic analyses were performed. PCR and western blot analyses were performed to detect the expression level of TPM1 and examine the related signalling pathway.
resultsThe IC DISCUSSION AND
conclusionsArecoline suppresses HaCaT cell viability by upregulating TPM1 through the TGF-β/Smad signalling pathway. This research provides a scientific basis for further study of arecoline and TPM1 in OSF and can be generalised to broader pharmacological studies. TPM1 may be a promising molecular target for treating OSF.
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