Long non-coding RNA HCP5 affects ferroptosis in lung adenocarcinoma cells through miR-17-5p/HOXA7 axis

Abstract

Abstract Background Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer. Ferroptosis is considered as a new target for the treatment of LUAD. Therefore, based on the previous bioinformatics mining of the ceRNA (competitive endogenous RNA) network human leukocyte antigen complex P5 (HCP5)/miR-17-5p/ Homeobox A7 (HOXA7) related to ferroptosis in LUAD, in this study, we verified the relationship between HCP5/miR-17-5p/HOXA7 axis and ferroptosis by cell experiments. Methods The dual luciferase report evaluated the interaction of HCP5 with miR-17-5p and miR-17-5p with HOXA7. Cell counting kit-8 (CCK-8) assay and transwell assay were used to detect the survival rate and invasion and migration of A549 cells, respectively. The ferroptosis-associated ACSL4 and SLC7A11, migration - and invasion-associated MMP9, vimentin, and E-cadherin proteins and mRNA were evaluated by Western blotting (WB) as well as real-time fluorescent quantitative PCR (qRT-PCR). Fe2+ and MDA were analyzed with kits. Results Overexpression of HCP5 promotes growth, proliferation, invasion and migration of A549 cells by increasing HOXA7 expression through regulation of miR-17-5P. In addition, knockdown of HCP5 elevated miR-17-5p and thus inhibited HOXA7 expression to suppress ferroptosis as well as epithelial mesenchymal transition in A549 cells. Conclusion Our results suggest that HCP5/miR-17-5p/HOXA7 can affect ferroptosis as well as biological behavior of A549 cells. Therefore, they can be considered as prognostic biomarkers and possible therapeutic targets for predicting the prognosis of LUAD.