Hsa-miR-1269a up-regulation fosters the malignant progression of esophageal squamous cell carcinoma via targeting FAM46C

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2023-07-01 DOI:10.1016/j.mrfmmm.2023.111832

Yuefeng Ma , Xin Xing , Chuantao Cheng , Ranran Kong , Liangzhang Sun , Feng Zhao , Danjie Zhang , Jianzhong Li

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引用次数: 0

Abstract

Esophageal squamous cell carcinoma (ESCC) is a malignancy of the alimentary tract resulting in death worldwide. The role and underlying mechanism of hsa-miR-1269a in the progression of ESCC remain unclear. In this study, hsa-miR-1269a was screened by differential expression analysis in TCGA, and its target gene FAM46C was predicted. qRT-PCR was conducted to assay the expression of hsa-miR-1269a and FAM46C in ESCC cells. The results showed that hsa-miR-1269a was upregulated in ESCC tissues and cell lines. Hsa-miR-1269a overexpression stimulated the proliferation, migration, and invasion capacities of ESCC cells, and FAM46C overexpression inhibited these phenotypes. Dual-luciferase assay verified that hsa-miR-1269a could target FAM46C. Next, qRT-PCR and western blot demonstrated that hsa-miR-1269a overexpression downregulated FAM46C. Rescue experiments revealed that hsa-miR-1269a accelerated the malignant progression of ESCC through FAM46C down-regulation. These results indicate that the interaction between hsa-miR-1269a and FAM46C plays a regulatory role in driving the malignant progression of ESCC cells, thereby providing a novel molecular mechanism for understanding ESCC.

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Hsa-miR-1269a上调通过靶向FAM46C促进食管鳞状细胞癌的恶性进展

食管鳞状细胞癌（ESCC）是一种在世界范围内导致死亡的消化道恶性肿瘤。hsa-miR-1269a在ESCC进展中的作用和潜在机制尚不清楚。在本研究中，通过TCGA中的差异表达分析筛选了hsa-miR-1269a，并预测了其靶基因FAM46C。qRT-PCR检测hsa-miR-1269a和FAM46C在ESCC细胞中的表达。结果表明，hsa-miR-1269a在ESCC组织和细胞系中上调。Hsa-miR-1269a过表达刺激ESCC细胞的增殖、迁移和侵袭能力，而FAM46C过表达抑制了这些表型。双荧光素酶检测证实hsa-miR-1269a可以靶向FAM46C。接下来，qRT-PCR和蛋白质印迹显示hsa-miR-1269a过表达下调FAM46C。拯救实验表明，hsa-miR-1269a通过下调FAM46C加速ESCC的恶性进展。这些结果表明，hsa-miR-1269a和FAM46C之间的相互作用在驱动ESCC细胞的恶性进展中起着调节作用，从而为理解ESCC提供了一种新的分子机制。

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

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.