LMOD1 Exerts a Tumor-Suppressive Role in Breast Cancer by Restraining the JAK2/STAT3 Pathway

IF 3.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Xiansong Fang, Xiaoyun Wen, Ya Hou, Liang Zhou, Yingjie Jiang, Yu Chen
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引用次数: 0

Abstract

Breast cancer has seriously affected women's physical and mental health. This investigation aims at screening differentially expressed genes (DEGs) in breast cancer and illuminating the potential biological functions of Leiomodin 1 (LMOD1) and its behind mechanisms against breast cancer. The common DEGs (co-DEGs) between the GSE22820 and GSE29431 data sets and pivotal genes were screened out using bioinformatics methods. The biological roles of LMOD1 overexpression on malignant phenotypes were validated by functional assays and the impact on fatty acid synthesis was also elucidated in breast cancer cell lines. Additionally, colivelin, a STAT3 activator, was applied for further investigating the role of LMOD1 on the JAK2/STAT3 pathway in vitro. A total of 208 co-DEGs and 5 focal genes were screened through bioinformatics analysis, and 5 focal genes were downregulated in breast cancer cell lines. LMOD1 overexpression retarded proliferative, migratory, invasive capabilities of breast cancer cells. LMOD1 overexpression suppressed fatty acid synthesis. Furthermore, the inhibitory effects on malignant phenotypes of breast cancer cells with LMOD1 overexpression were partially abolished after colivelin treatment. Additionally, LMOD1 could impede fatty acid synthesis in breast cancer cells. Our study highlighted LMOD1 exerted as a tumor-suppressive role in breast cancer, which was correlated with restraining the JAK2/STAT3 pathway activation.

Abstract Image

乳腺癌严重影响妇女的身心健康。本研究旨在筛选乳腺癌中的差异表达基因(DEGs),揭示雷欧莫定1(LMOD1)的潜在生物学功能及其对抗乳腺癌的机制。利用生物信息学方法筛选出了GSE22820和GSE29431数据集之间的共同DEGs(co-DEGs)和关键基因。通过功能试验验证了 LMOD1 过表达对恶性表型的生物学作用,并阐明了其对乳腺癌细胞系脂肪酸合成的影响。此外,为了进一步研究 LMOD1 在体外 JAK2/STAT3 通路中的作用,还应用了 STAT3 激活剂可乐定。通过生物信息学分析,共筛选出208个共DEGs和5个焦点基因,其中5个焦点基因在乳腺癌细胞系中下调。LMOD1过表达会抑制乳腺癌细胞的增殖、迁移和侵袭能力。LMOD1 的过表达抑制了脂肪酸的合成。此外,LMOD1 过表达对乳腺癌细胞恶性表型的抑制作用在可乐定处理后部分消失。此外,LMOD1 还能阻碍乳腺癌细胞中脂肪酸的合成。我们的研究强调了 LMOD1 在乳腺癌中的抑瘤作用,这与抑制 JAK2/STAT3 通路的激活有关。
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来源期刊
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.
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