Quercetin Inhibits the Epithelial to Mesenchymal Transition through Suppressing Akt Mediated Nuclear Translocation of β-Catenin in Lung Cancer Cell Line.
Perumal ElumalaiEzhilarasan DevarajRaghunandha Kumar SubramanianPublished in: Nutrition and cancer (2021)
Lung cancer is a first leading cause of cancer related death worldwide. Quercetin (QUE) has chemo-preventive effect against a variety of cancers. However, the molecular mechanism of QUE mediated inhibition of cancer cell migration and epithelial to mesenchymal transition (EMT) is not clear in lung cancer. Therefore, this study investigates the effect of QUE on EMT and metastasis of lung cancer cell line (A549). The MTT assay, scratch wound healing assay, Transwell migration and invasion assay performed to assess the cell viability and migration potential of lung cancer cells after treatment with different concentration of QUE. Further, chemokines gene expression was analyzed by qPCR and EMT markers were analyzed by immunocytochemistry and Western blot. QUE inhibits cell viability in a dose-dependent (10-80 μM) manner both at 24 and 48 h treatment. The Akt/MAPK/β-catenin and EMT marker protein expressions were decreased significantly, whereas TIMP-2 expression was increased upon QUE treatment. QUE inhibits cell migration and invasion of A-549 cells. In addition, Immunocytochemistry result showed that QUE can reduce nuclear translocalisation of β-catenin in A549 cells. Our results suggest that QUE can inhibit the metastatic potential in lung cancer by altering the Akt/MAPK/β-catenin signaling pathway and inhibiting the nuclear translocation of β-catenin.
Keyphrases
- epithelial mesenchymal transition
- signaling pathway
- induced apoptosis
- cell proliferation
- pi k akt
- gene expression
- cell cycle arrest
- cell migration
- high throughput
- poor prognosis
- dna methylation
- squamous cell carcinoma
- wound healing
- single cell
- papillary thyroid
- stem cells
- cell therapy
- small molecule
- south africa
- young adults
- drug delivery
- squamous cell
- mesenchymal stem cells
- protein protein
- locally advanced
- replacement therapy