ArticleOncology letters2023
Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway.
Article in Oncology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Exploration of the mechanism of hesperidin inhibition on the proliferation and metastasis of human breast cancer cells.International journal of clinical and experimental pathology · 2026Article
- Orchestration of the tumor microenvironment by citrus flavonoids: from preclinical mechanisms to translational therapeutic.Frontiers in immunology · 2026Review
- Hesperidin Inhibits Proliferation and Metastasis of Human Breast Cancer Cells by Suppressing MMP-2/9 Activity and Reversing Epithelial-Mesenchymal Transition.Cancer informatics · 2026Article
- Exosomes derived from M2 macrophages regulate airway inflammation by modulating epithelial cell proliferation and apoptosis.Journal of inflammation (London, England) · 2025Article
- Glucosyl Hesperidin Supplementation Prevents Tubulointerstitial Fibrosis and Immune Activation in Diabetic Nephropathy in Mice.Nutrients · 2025Article
- As shown hesperidin suppresses TGF-β2-induced proliferation and epithelial-mesenchymal transition of retinal pigment epithelial cells.Journal of molecular histology · 2024Article
- Machine Learning Reveals Impacts of Smoking on Gene Profiles of Different Cell Types in Lung.Life (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tobacco smoke (TS) is the major cause of lung cancer. The abnormal proliferation and epithelial-mesenchymal transition (EMT) of lung cells promote occurrence and development of lung cancer. The p38 pathway intervenes in this cancer development. Hesperidin also serves a role in human health and disease prevention. The roles of p38 in TS-mediated abnormal cell proliferation and EMT, and the hesperidin intervention thereof are not yet understood. In the present study, it was demonstrated that TS upregulated proliferating cell nuclear antigen, vimentin and N-cadherin expression, whereas it downregulated E-cadherin expression, as assessed using western blotting and reverse transcription-quantitative PCR. Furthermore, it was observed that inhibition of the p38 pathway inhibit TS-induced proliferation and EMT. Hesperidin treatment prevented the TS-induced activation of the p38 pathway, EMT and cell proliferation in mouse lungs. The findings of the present study may provide insights into the pathogenesis of TS-related lung cancer.
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Registered trials
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