The mechanism of lovastatin in suppressing the proliferation of esophageal squamous cell carcinoma based on proteomics

IF 3.2 4区医学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Journal of Gene Medicine Pub Date : 2024-08-08 DOI:10.1002/jgm.3722

Feng Peng, Lili Zhu, Jiang Fan, Fu Yang

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引用次数: 0

Abstract

Background

Lovastatin, a type of statin usually considered as a lipid-lowering drug that lowers blood cholesterol and low-density lipoprotein cholesterol levels, has been rediscovered to have anticancer activity. Fewer studies exist regarding the effect of lovastatin on esophageal squamous cell carcinoma (ESCC).

Methods

Here, we report that lovastatin shows anticancer effect on ESCC By affecting the mitochondrial autophagy pathway. Moreover, based on proteomics and computer molecular simulations found that RAB38 and RAB27A may be a target of lovastatin.

Results

We observed that autophagy of mitochondria is inhibited by lovastatin, affecting esophageal squamous cell proliferation. There is a possible link between the expression of RAB38, RAB27A and immune cell invasion in esophageal cancer.

Conclusions

These results demonstrate the huge potential of lovastatin as an RAB38, RAB27A inhibitor in esophageal cancer chemotherapy and chemoprevention.

Abstract Image

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基于蛋白质组学研究洛伐他汀抑制食管鳞癌增殖的机制

背景：洛伐他汀是一种他汀类药物，通常被认为是一种降脂药物，可降低血液中胆固醇和低密度脂蛋白胆固醇的水平。方法：在此，我们报告了洛伐他汀通过影响线粒体自噬途径对食管鳞状细胞癌（ESCC）的抗癌作用。此外，基于蛋白质组学和计算机分子模拟发现，RAB38和RAB27A可能是洛伐他汀的靶点：结果：我们观察到洛伐他汀抑制了线粒体的自噬，从而影响了食管鳞状细胞的增殖。RAB38、RAB27A的表达与食管癌免疫细胞侵袭之间可能存在联系：这些结果表明，洛伐他汀作为一种 RAB38、RAB27A 抑制剂，在食管癌化疗和化学预防方面具有巨大潜力。

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

Journal of Gene Medicine 医学-生物工程与应用微生物

CiteScore

6.40

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The aims and scope of The Journal of Gene Medicine include cutting-edge science of gene transfer and its applications in gene and cell therapy, genome editing with precision nucleases, epigenetic modifications of host genome by small molecules, siRNA, microRNA and other noncoding RNAs as therapeutic gene-modulating agents or targets, biomarkers for precision medicine, and gene-based prognostic/diagnostic studies. Key areas of interest are the design of novel synthetic and viral vectors, novel therapeutic nucleic acids such as mRNA, modified microRNAs and siRNAs, antagomirs, aptamers, antisense and exon-skipping agents, refined genome editing tools using nucleic acid /protein combinations, physically or biologically targeted delivery and gene modulation, ex vivo or in vivo pharmacological studies including animal models, and human clinical trials. Papers presenting research into the mechanisms underlying transfer and action of gene medicines, the application of the new technologies for stem cell modification or nucleic acid based vaccines, the identification of new genetic or epigenetic variations as biomarkers to direct precision medicine, and the preclinical/clinical development of gene/expression signatures indicative of diagnosis or predictive of prognosis are also encouraged.