Long Non-Coding RNA HCP5 Affects Ferroptosis in Lung Adenocarcinoma through miR-17-5p/HOXA7 Axis

Background: Ferroptosis, a regulated cell death initiated by Fe-dependent lipoperoxidation, is closely linked to the development of lung adenocarcinoma (LUAD). LncRNA human leukocyte antigen complex P5 (HCP5) has been confirmed as oncogenic in LUAD, but its function in ferroptosis is unknown. Objective: Based on the previous bioinformatics mining of the ceRNA (competitive endoge-nous RNA) network HCP5/miR-17-5p/ Homeobox A7 (HOXA7) related to ferroptosis in LUAD, in this study, we characterized the cell-based experiments to validate the binding be-tween the HCP5/miR-17-5p/HOXA7 axis and ferroptosis. Methods: The HCP5/miR-17-5p/HOXA7 linkage was identified by a two-luciferase reporter. Cell Counting Kit-8 (CCK-8) and Transwell assay were employed for the detection of viabil-ity, invasion, and migration of A549 cells, respectively. ACSL4 and SLC7A11 were associat-ed with ferroptosis, MMP 9, vimentin, and E-cadherin, which were associated with migration and invasion and were assessed by WB and qRT-PCR. Fe2+ and malondialdehyde (MDA) were analyzed using kits. Results: Over-expression of HCP5 enhances the growth, invasion, and migration of A549 cells by adjusting miR-17-5P to increase the expression of HOXA7. In addition, the knock-down of HCP5 elevated miR-17-5p, which inhibited HOXA7 expression and suppressed fer-roptosis and EMT in A549 cells. Conclusion: HCP5/miR-17-5p/HOXA7 can affect ferroptosis as well as the biological behav-ior of A549 cells.