Interferon Induced Upregulation of Tripartite Motif 34 (TRIM34) Leads Apoptotic Cell Death in Lung Adenocarcinoma

IF 3.2 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-28 DOI:10.1002/jbt.70072

Kaushalkumar Chaudhari, Vihas T. Vasu, Aparna Golani, Afridi Shaikh, Nidhi Nagariya, Hetal Roy

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Abstract

Despite breakthroughs in our understanding of lung cancer risk, development, immunologic control, and therapy choices, it remains one of the leading causes of cancer mortality. This study aimed to investigate the role of TRIM34 upon treatment of Interferon Gamma (IFN-γ) in Non-Small Cell Lung Cancer (NSCLC). NCI-H23 cells were exposed to IFN-γ in a dose- and time-dependent manner to understand TRIM34 expression and its role as a co-regulator of treatment. The regulatory role of TRIM34 on IFN-γ exposure was studied by qRT-PCR, Western blot analysis, immunocytochemistry, apoptosis assay and scratch assay. On exposure to IFN-γ, TRIM34 expression at transcript and protein level was significantly upregulated. With its upregulation, NCI-H23 underwent apoptosis and its rate of proliferation was impeded. Our results suggest that induction of TRIM34 by IFN-γ treatment may lead to an anti-tumor inflammatory response, resulting in NSCLC regression via apoptosis.

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干扰素诱导的三方基质 34 (TRIM34) 上调导致肺腺癌细胞凋亡

尽管我们对肺癌风险、发展、免疫学控制和治疗选择的认识取得了突破性进展，但肺癌仍然是导致癌症死亡的主要原因之一。本研究旨在探究 TRIM34 在非小细胞肺癌（NSCLC）γ 干扰素（IFN-γ）治疗中的作用。研究人员以剂量和时间依赖性的方式让NCI-H23细胞暴露于IFN-γ，以了解TRIM34的表达及其作为治疗共同调节因子的作用。研究人员通过 qRT-PCR、Western 印迹分析、免疫细胞化学、细胞凋亡检测和划痕检测研究了 TRIM34 对 IFN-γ 暴露的调控作用。暴露于 IFN-γ 后，TRIM34 在转录本和蛋白水平的表达均显著上调。随着TRIM34表达的上调，NCI-H23出现凋亡，其增殖速度也受到阻碍。我们的研究结果表明，IFN-γ治疗诱导TRIM34可能会导致抗肿瘤炎症反应，从而通过细胞凋亡使NSCLC消退。

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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.