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

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.

Machine Learning Reveals Impacts of Smoking on Gene Profiles of Different Cell Types in Lung

“…Furthermore, smoking systemically incites chronic inflammation in the lungs, potentially stimulating pathways that elevate FOS (c-Fos) expression as a cellular countermeasure [95,96]. One particular study underscored that the anomalous lung epithelial-mesenchymal transition and cell proliferation due to tobacco smoke were linked to the up-regulation of phosphorylated p38 and phosphorylated c-Fos, substantiating the relationship between FOS expression and smoking [97]. Hence, FOS is instrumental as a key parameter in formulating rules to ascertain smoking status.…”