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

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-10-21 DOI:10.2174/0115680096321714240909182553

Qingyun Pan, Zige Tang, Jiayu Zheng, Lingxin Yan, Quanfang Chen

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Abstract

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 endogenous 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 between 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 viability, invasion, and migration of A549 cells, respectively. ACSL4 and SLC7A11 were associated 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 ferroptosis and EMT in A549 cells.

Conclusion: HCP5/miR-17-5p/HOXA7 can affect ferroptosis as well as the biological behavior of A549 cells.

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长非编码 RNA HCP5 通过 miR-17-5p/HOXA7 轴影响肺腺癌的铁突变性

背景：铁过氧化是一种由铁依赖性脂过氧化引发的调节性细胞死亡，与肺腺癌（LUAD）的发生密切相关。LncRNA 人类白细胞抗原复合物 P5（HCP5）已被证实在 LUAD 中具有致癌作用，但其在铁氧化过程中的功能尚不清楚：目的：基于之前对LUAD中与铁突变相关的ceRNA（竞争性内源性RNA）网络HCP5/miR-17-5p/HOXA7（Homeobox A7）的生物信息学挖掘，本研究通过基于细胞的实验来验证HCP5/miR-17-5p/HOXA7轴与铁突变之间的结合：方法：HCP5/miR-17-5p/HOXA7 连接是通过双荧光素酶报告物确定的。细胞计数试剂盒-8（CCK-8）和 Transwell 试验分别用于检测 A549 细胞的活力、侵袭和迁移。ACSL4和SLC7A11与铁突变相关，MMP 9、波形蛋白和E-cadherin与迁移和侵袭相关，并通过WB和qRT-PCR进行了评估。用试剂盒分析了Fe2+和丙二醛（MDA）：结果：通过调节 miR-17-5P 增加 HOXA7 的表达，过度表达 HCP5 可增强 A549 细胞的生长、侵袭和迁移。此外，敲除 HCP5 会升高 miR-17-5p，从而抑制 HOXA7 的表达，抑制 A549 细胞的铁突变和 EMT：结论：HCP5/miR-17-5p/HOXA7可影响A549细胞的铁突变及生物学行为。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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