Abstract
The tumor-suppressing role of miR-455-3p has been reported in lung cancer, but the working mechanism remains to be fully elucidated. This study aims to explore the possible mechanism of miR-455-3p in regulating epithelial–mesenchymal transition (EMT) progression and angiogenesis in non-small cell lung cancer (NSCLC) cells.
The expressions of miR-455-3p, HSF1, GLS1, and EMT-related proteins (E-cadherin, N-cadherin, vimentin, and Snail-1) in both NSCLC tissues and cell lines were determined by RT-qPCR and western blot. After cell transfection, cell proliferation and angiogenesis ability on NSCLC cells were assessed by MTT and tube formation assay. The binding of miR-455-3p with HSF1 was measured by luciferase reporter gene assay, while the interaction between HSF1 and GLS1 was determined by co-immunoprecipitation assay (Co-IP).
HSF1 was highly expressed in NSCLC tissues and cells. Inhibition of HSF1 expression or overexpression of miR-455-3p in NSCLC cells can suppress cell proliferation, angiogenesis ability, and EMT progression. miR-455-3p was found to negatively regulate HSF1 expression. Co-transfection of miR-455-3p overexpression and HSF1 inhibition in NSCLC cells showed that miR-455-3p can partially counteract the effect of HSF1 in NSCLC cells. HSF1 can interact with GLS1 and elevate the expression of GLS1. GLS1 can partially abolish the suppressive effect of miR-455-3p in NSCLC cells.
miR-455-3p can bind HSF1 to suppress the GLS1 in NSCLC cells, therefore suppressing EMT progression and angiogenesis of NSCLC cells.
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The datasets used or analyzed during the current study are available from the corresponding author on reasonable request.
Change history
16 February 2022
A Correction to this paper has been published: https://doi.org/10.1007/s12192-022-01259-z
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Meng, C., Liu, K., Cai, X. et al. Mechanism of miR-455–3 in suppressing epithelial–mesenchymal transition and angiogenesis of non-small cell lung cancer cells. Cell Stress and Chaperones 27, 107–117 (2022). https://doi.org/10.1007/s12192-022-01254-4
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DOI: https://doi.org/10.1007/s12192-022-01254-4