FHOD3 Promotes the Progression of Lung Cancer by Regulating the Caspase-3-Mediated Signaling Pathway.

IF 2.3 4区医学 Q3 ONCOLOGY

Current cancer drug targets Pub Date : 2024-10-18 DOI:10.2174/0115680096330059240909172011

Zhonglu Peng, Junjie Wang, Zhenghang Huan, Chengmin Zhou, Zhifeng Li, Huilong Fang, Zhiying Yang, Dongyang He, Weiquan Xie

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引用次数: 0

Abstract

Introduction/objective: Lung cancer causes hundreds of thousands of deaths each year worldwide. FHOD3 was reported to accelerate the progression of brain cancer. However, its role in lung cancer is not clear. This study aimed to investigate the role of FHOD3 in lung cancer.

Methods: The clinical significance of FHOD3 in lung cancer was analyzed based on the data from the TCGA database. The expression level of FHOD3 was detected by qPCR technology. Cell proliferation was detected by CCK-8 assay, and cell invasion was detected by transwell assay. The activity of caspase-3 was determined by the ELISA method, cell apoptosis was iden-tified by TUNEL assay, and protein expression was measured by western blotting technology.

Results: Based on the TCGA data, FHOD3 was overexpressed in tumor tissues compared to the normal tissues. Patients with higher FHOD3 expression exhibited a worse survival rate. The expression levels of FHOD3 in lung cancer cell lines were much higher than that in normal cells. When FHOD3 was knocked down, the ability of cell proliferation and invasion was sig-nificantly inhibited. Cell apoptosis rate was increased reversely. The activity of caspase-3 was increased significantly. In addition, the expression level of cleaved caspase-3 was increased. The expression levels of Bax, caspase-8, and ICAD were also increased significantly. However, the expression of antiapoptotic molecule Bcl-2 was decreased reversely. This suggests that the caspase-3-mediated apoptosis signaling pathway was activated by FHOD3 knockdown.

Conclusion: FHOD3 was overexpressed and negatively associated with survival rate in lung cancer patients. FHOD3 regulates cell proliferation, invasion, and apoptosis through the caspase-3-mediated signaling pathway. This study indicates that FHOD3 is an important gene contributing to the progression of lung cancer and might be a new drug target for the therapy of lung cancer.

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FHOD3 通过调控 Caspase-3 介导的信号通路促进肺癌进展

导言/目的：全世界每年有数十万人死于肺癌。据报道，FHOD3 可加速脑癌的进展。然而，它在肺癌中的作用尚不明确。本研究旨在探讨 FHOD3 在肺癌中的作用：方法：基于 TCGA 数据库的数据，分析 FHOD3 在肺癌中的临床意义。采用 qPCR 技术检测 FHOD3 的表达水平。细胞增殖采用 CCK-8 法检测，细胞侵袭采用 transwell 法检测。ELISA法测定Caspase-3的活性，TUNEL法鉴定细胞凋亡，Western印迹技术检测蛋白表达：结果：根据TCGA数据，与正常组织相比，FHOD3在肿瘤组织中表达过高。FHOD3表达较高的患者生存率较低。FHOD3在肺癌细胞系中的表达水平远高于正常细胞。当 FHOD3 被敲除后，细胞的增殖和侵袭能力受到显著抑制。细胞凋亡率反向增加。Caspase-3 的活性明显增加。此外，已裂解的 caspase-3 的表达水平也有所增加。Bax、caspase-8 和 ICAD 的表达水平也明显增加。然而，抗凋亡分子 Bcl-2 的表达却反向下降。这表明 FHOD3 基因敲除激活了 caspase-3 介导的细胞凋亡信号通路：结论：FHOD3过表达与肺癌患者的生存率呈负相关。结论：FHOD3 的高表达与肺癌患者的生存率呈负相关，FHOD3 通过 Caspase-3 介导的信号通路调节细胞增殖、侵袭和凋亡。这项研究表明，FHOD3 是导致肺癌进展的重要基因，可能成为治疗肺癌的新药靶点。

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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来源期刊

Current cancer drug targets 医学-肿瘤学

CiteScore

5.40

自引率

0.00%

发文量

105

审稿时长

1 months

期刊介绍： Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes and genes. Current Cancer Drug Targets publishes original research articles, letters, reviews / mini-reviews, drug clinical trial studies and guest edited thematic issues written by leaders in the field covering a range of current topics on drug targets involved in cancer. As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.