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IF 3.2 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-12-18 DOI:10.1002/jbt.70087

Xinyu Luan, Xuxing Peng, Gang Hui, Zichun Wei

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引用次数: 0

摘要

肺腺癌（LUAD）是一种常见的肺癌，病理机制复杂。转录因子AP-2 Alpha（TFAP2A）和半胱氨酸蛋白酶抑制剂1（CST1）是LUAD样本中的上调基因，因此我们重点研究TFAP2A/CST1轴在LUAD中的作用。表达分析采用实时定量聚合酶链反应和 Western 印迹法进行。细胞行为通过集落形成试验、EdU 试验、伤口愈合试验和流式细胞术进行检测。铁变态反应通过氧化指标、Fe2+水平和相关蛋白进行评估。通过 ChIP 检测和双荧光素酶报告实验分析了 TFAP2A 和 CST1 的相互作用。异种移植肿瘤实验评估了 TFAP2A 在体内的功能。CST1 在 LUAD 样本和细胞中过表达。下调 CST1 可抑制 LUAD 细胞的增殖和迁移，但可促进其凋亡和铁凋亡。TFAP2A 与 CST1 的启动子相互作用，上调 CST1 的表达。TFAP2A通过靶向CST1调控LUAD细胞的恶性行为和铁凋亡。TFAP2A 通过介导 CST1 影响 LUAD 肿瘤的生长。所有这些数据证明，TFAP2A/CST1轴促进了LUAD细胞的增殖和迁移，同时抑制了细胞凋亡和铁凋亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

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TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

Lung adenocarcinoma (LUAD) is a common type of lung cancer with complicated pathological mechanism. Transcription Factor AP-2 Alpha (TFAP2A) and Cysteine protease inhibitor 1 (CST1) are upregulated genes in LUAD samples, accordingly, we focused on clarifying the role of TFAP2A/CST1 axis in LUAD. Expression analysis was performed using real-time quantitative polymerase chain reaction and western blot. Cellular behaviors were detected by colony formation assay, EdU assay, wound healing assay and flow cytometry. Ferroptosis was assessed by oxidative indicators, Fe²⁺ level and related proteins. TFAP2A and CST1 interaction was analyzed via ChIP assay and dual-luciferase reporter assay. TFAP2A function in vivo was evaluated by xenograft tumor assay. CST1 was overexpressed in LUAD samples and cells. Downregulation of CST1 inhibited proliferation, migration but it promoted apoptosis and ferroptosis of LUAD cells. TFAP2A interacted with the promoter of CST1 to up-regulate CST1 expression. TFAP2A regulated the malignant behaviors and ferroptosis of LUAD cells by targeting CST1. TFAP2A affected LUAD tumor growth via mediating CST1. All these data proved that TFAP2A/CST1 axis contributed to proliferation, migration while it suppressed apoptosis and ferroptosis in LUAD.

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来源期刊

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.