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ArticleCurrent cancer drug targets2025

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

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

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Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Qingyun PanDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, Guangxi, China.ORCID 0000-0002-4441-6396
Zige TangDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, Guangxi, China.
Jiayu ZhengDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, Guangxi, China.
Lingxin YanDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, Guangxi, China.
Quanfan ChenDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, Guangxi, China.

Funding

Guangxi Medical University "Medical Excellence Award"National Natural Science Foundation of China 82360540
6 · The paper itself

Abstract

backgroundFerroptosis, 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.

objectiveBased 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.

methodsThe 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.

resultsOver-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 knockdown of HCP5 elevated miR-17-5p, which inhibited HOXA7 expression and suppressed ferroptosis and EMT in A549 cells.

conclusionHCP5/miR-17-5p/HOXA7 can affect ferroptosis as well as the biological behavior of A549 cells.

Indexed as

Adenocarcinoma of LungFerroptosisHomeodomain ProteinsLung NeoplasmsMicroRNAsRNA, Long NoncodingA549 CellsCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansHCP5 long noncoding RNA, humanHomeodomain ProteinsMicroRNAsMIRN17 microRNA, humanRNA, Long Noncodingferroptosishcp5hoxa7Lung adenocarcinomamiR-17-5ptherapeutic targets.

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.