TGF-β1/miR-30d-5p axis regulating the expression of EMT key factors to induce apoptosis of lung cancer cells

Previous studies have reported that miR-30d-5p gene expression can inhibit tumor proliferation, but its mechanism has not been fully elucidated. Based on previous findings, TGF-β1 was used to induce epithelial mesenchymal transformation in A549 cells. The expression levels of DUSP-1, E-cadherin and...

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Veröffentlicht in:Heliyon 2024-09, Vol.10 (18), p.e37801, Article e37801
Hauptverfasser: Zeng, Qigang, Shi, Wenjie, Xie, Longyun, Dai, Yong, Wei, Chenggong
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Sprache:eng
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Zusammenfassung:Previous studies have reported that miR-30d-5p gene expression can inhibit tumor proliferation, but its mechanism has not been fully elucidated. Based on previous findings, TGF-β1 was used to induce epithelial mesenchymal transformation in A549 cells. The expression levels of DUSP-1, E-cadherin and Vimentin were detected by Western blot. mRNA expression levels of DUSP-1, E-cadherin and Vimentin were determined by RT-qPCR. The expression level of miR-30d-5p was determined by RT-qPCR. The induction effect of TGF-β1 could be reversed by the intervention of miR-30d-5p in A549 cells. miRNA inhibition experiment showed that miR-30d-5p inhibitor could effectively inhibit the expression of miR-30d-5p in A549 cells. After miR-30d-5p intervention, TGF-β1 was reversed on EMT-related genes (Dusp-1, E-cadherin, Vimentin). TGF-β1 can induce epithelial mesenchymal transformation of A549 cells, and miR-30d-5p may be a key regulatory mechanism in regulating gene and protein expression of TGF-β1-mediated DUSP-1, E-cadherin and Vimentin. This provides a new perspective for understanding the anti-tumor effect of miR-30d-5p gene.
ISSN:2405-8440
2405-8440
DOI:10.1016/j.heliyon.2024.e37801