miR-129-2-3p 与 SEMA4C 结合，调控 HCC 的发展并抑制 EMT

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2024-07-01 DOI:10.1016/j.mrfmmm.2024.111872

Siyuan Ma , Chun Pu

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引用次数: 0

摘要

背景在原发性肝癌中，HCC 的发病率最高。方法使用 RT-qPCR 评估 miR-129-2-3p 和 SEMA4C 的表达水平。CCK-8、侵袭和伤口愈合试验分别用于确认 HCC 细胞的增殖、侵袭和迁移能力。通过 ELISA 检测血清 SEMA4C 水平。RIP和双荧光素酶报告实验用于确认基因间结合位点的存在。细胞凋亡检测和细胞周期检测用于检测细胞的凋亡率和周期分布，WB检测SEMA4C、RhoA、ROCK1、E-cadherin、N-cadherin和vimentin的蛋白表达。此外，动物实验进一步证实了 miR-129-2-3p 的抑癌作用。过表达 miR-129-2-3p 会降低 HCC 细胞的增殖、侵袭、迁移和 EMT，而抑制 miR-129-2-3p 则会产生相反的效果。我们的研究还表明，SEMA4C 在 HCC 组织、血清和细胞中均有增高，而 SEMA4C 的敲除可阻止 HCC 细胞的侵袭、迁移、增殖和 EMT。结论总之，我们发现 miR-129-2-3p 通过与 SEMA4C 结合，调控 HCC 细胞的增殖、侵袭、迁移和 EMT。

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miR-129–2-3p binds SEMA4C to regulate HCC development and inhibit the EMT

Background

Among primary liver cancers, HCC is the most prevalent. Small noncoding RNAs called miRNAs control the expression of downstream target genes to take part in a variety of physiological and pathological processes, including those related to cancer.

Methods

miR-129–2–3p and SEMA4C expression levels were assessed using RT-qPCR. The CCK-8, invasion, and wound healing assays were used to confirm the capacity of HCC cells for proliferation, invasion and migration respectively. Serum SEMA4C levels were detected via ELISA. The RIP and dual-luciferase reporter assays were used to confirm the existence of intergenic binding sites. Cell apoptosis assay and cell cycle assay were performed to detect the apoptosis rate and cycle distribution of cells, and WB was performed to detect the protein expression of SEMA4C, RhoA, ROCK1, E-cadherin, N-cadherin, and vimentin. Furthermore, cancer-inhibiting role of miR-129–2–3p were further confirmed by animal tests.

Results

miR-129–2–3p expression was reduced in HCC tissues and cells. Overexpression of miR-129–2–3p decreased the proliferation, invasion, migration, and EMT in HCC cells, whereas inhibition of miR-129–2–3p had the opposite effects. Our research also showed that SEMA4C was increased in HCC tissues, serum and cells, and that SEMA4C knockdown prevented HCC cell invasion, migration, proliferation, and EMT. Overexpression of SEMA4C reversed the inhibitory effect of miR-129–2–3p on HCC.

Conclusions

Overall, we discovered that through binding to SEMA4C, miR-129–2–3p regulates HCC cell proliferation, invasion, migration, and EMT.

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来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.