Fisetin suppresses cigarette smoke extract-induced epithelial to mesenchymal transition of airway epithelial cells through regulating COX-2/MMPs/β-catenin pathway

Agraval, Hina; Sharma, Jiten R.; Prakash, Nutan; Yadav, Umesh C. S.

doi:10.1016/j.cbi.2021.109771

Cited by 10 publications

(5 citation statements)

References 51 publications

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“…MMP9 is a matrix metallopeptidase elevated in the plasma of patients with severe COVID-19 and correlated with in-hospital deaths [ 97 ]. Upregulation of MMP9 by CS [ 70 , 74 , 98 – 101 ] and EC+N [ 49 ] suggests an increased risk of developing severe COVID-19. The downregulation of MMP9 following exposure to EC−N [ 49 ] implies no additional risk for those using nicotine-free e-cigarettes and indicates a role for nicotine in MMP9 expression.…”

Section: Discussionmentioning

confidence: 99%

Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis

Bowsher,

Marczylo,

Gooch

et al. 2024

Eur Respir J

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Evidence for the impact of smoking on COVID-19 is contradictory, and there is little research on vaping. Here we provide greater clarity on mechanisms perturbed by tobacco cigarette, electronic cigarette and nicotine exposures that may impact the risks of infection and/or disease severity.Following PRISMA guidelines, OVID and Web of Science databases were searched. Study design and exposure-induced gene expression changes were extracted. Each study was quality assessed and higher confidence scores were assigned to genes consistently changed across multiple studies following the same exposure. These genes were used to explore pathways significantly altered following exposure.125 studies provided data on 480 genes altered by exposure to tobacco cigarettes, e-cigarettes, nicotine or SARS-CoV-2. Genes involved in both SARS-CoV-2 viral-entry and inflammation were changed following exposure. Pathway analysis revealed that many of those genes with high confidence scores are involved in common cellular processes relating to hyperinflammatory immune responses.Exposure to tobacco cigarettes, e-cigarettes, or nicotine, may therefore impact initial host-pathogen interactions and disease severity. Smokers and vapers of e-cigarettes with nicotine, could potentially be at increased risk of SARS-CoV-2 infection, associated cytokine storm, and acute respiratory distress syndrome. However, further research is required, particularly on e-cigarettes, to determine the biological mechanisms involved in perturbation of viral-entry genes and host-pathogen interactions and subsequent responses within the respiratory tract. This will improve our physiological understanding of the impact of smoking and vaping on COVID-19, informing public health advice and providing improved guidance for management of SARS-CoV-2 and other respiratory viruses.

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Section: Discussionmentioning

confidence: 99%

Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis

Bowsher,

Marczylo,

Gooch

et al. 2024

Eur Respir J

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“…Carcinogens can stimulate abnormal cell proliferation and EMT, leading to lung cancer ( 10 – 12 ). TS-induced abnormal EMT and cell proliferation regulate early events in cancer ( 54 – 56 ). In the present study, the change in the expression levels of EMT and proliferation markers indicated abnormal EMT and cell proliferation in the lungs of mice exposed to TS.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Liang

Zhang

et al. 2022

Oncol Lett

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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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“…Furthermore, reactivated epithelial–mesenchymal transition (EMT) often facilitates the metastatic spread of cancer cells, which is a process where fully differentiated epithelial cells undergo a transition to poorly differentiated and migratory mesenchymal cells [ 41 , 42 ]. Fisetin has been shown to have the ability to reverse EMT, thereby inhibiting the invasion and migration of cancer cells [ 43 ].…”

Section: Biological Function Of Fisetin (Fig 1 )mentioning

confidence: 99%

Biological effects and mechanisms of fisetin in cancer: a promising anti-cancer agent

Zhou,

Huang,

Nie

et al. 2023

Eur J Med Res

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Fisetin, a natural flavonoid, possesses numerous biological activities that have been extensively studied in various diseases. When it comes to cancer, fisetin exhibits a range of biological effects, such as suppressing cell growth, triggering programmed cell death, reducing the formation of new blood vessels, protecting against oxidative stress, and inhibiting cell migration. Moreover, fisetin has the ability to enhance the effectiveness of chemotherapy. The anticancer properties of fisetin can be attributed to a diverse array of molecules and signaling pathways, including vascular endothelial growth factor (VEGF), mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), PI3K/Akt/mTOR, and Nrf2/HO-1. Consequently, fisetin holds promise as a therapeutic agent for anticancer treatment. In this review, we place emphasis on the biological functions and various molecular targets of fisetin in anticancer therapy.

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Fisetin suppresses cigarette smoke extract-induced epithelial to mesenchymal transition of airway epithelial cells through regulating COX-2/MMPs/β-catenin pathway

Cited by 10 publications

References 51 publications

Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis

Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Biological effects and mechanisms of fisetin in cancer: a promising anti-cancer agent

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