HMMR在肺腺癌中的促瘤作用

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2023-01-01 DOI:10.1016/j.mrfmmm.2022.111811
Qihao Wang , Guomin Wu , Linhai Fu , Zhupeng Li , Yuanlin Wu , Ting Zhu , Guangmao Yu
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引用次数: 1

摘要

寻找肺腺癌(LUAD)的差异基因对研究至关重要。透明质酸介导的运动受体(HMMR)促进癌症患者的恶性进展。然而,HMMR介导的LUAD发病的分子调控因子尚不清楚。本工作旨在研究HMMR与LUAD细胞增殖、迁移和侵袭的相关性。评估LUAD细胞和HLF-a细胞中的Let-7c-5p和HMMR水平,并检测它们的相关性。通过双荧光素酶实验和qRT-PCR测定它们的相互作用。通过细胞计数试剂盒-8(CCK-8)、集落形成、划痕愈合和transwell分析验证了体外细胞增殖、迁移和侵袭潜力。通过qRT-PCR和蛋白质印迹检测HMMR的表达,并通过qRT-PCR检测let-7c-5p的表达。研究发现,LUAD患者HMMR水平升高,且与let-7c-5p水平呈负相关。Let-7c-5p直接靶向HMMR抑制LUAD细胞的增殖、迁移和侵袭。上述数据表明,let-7c-5p/HMMR轴可能为LUAD患者提供一定的治疗价值。
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Tumor-promoting roles of HMMR in lung adenocarcinoma

Searching for differential genes in lung adenocarcinoma (LUAD) is vital for research. Hyaluronan mediated motility receptor (HMMR) promotes malignant progression of cancer patients. However, the molecular regulators of HMMR-mediated LUAD onset are unknown. This work aimed to study the relevance of HMMR to proliferation, migration and invasion of LUAD cells. Let-7c-5p and HMMR levels in LUAD cells and HLF-a cells were assessed, and their correlation was also detected. Their interaction was determined by dual-luciferase experiments and qRT-PCR. Cell proliferation, migration and invasion potentials in vitro were validated through cell counting kit-8 (CCK-8), colony formation, scratch healing, and transwell assays. The expression of HMMR was examined by qRT-PCR and western blot and the expression of let-7c-5p was assayed by qRT-PCR. It was found that HMMR level was increased in LUAD and negatively correlated with let-7c-5p level. Let-7c-5p directly targeted HMMR to repress LUAD cell proliferation, migration and invasion. The above data illustrated that the let-7c-5p/HMMR axis may provide certain therapeutic value for LUAD patients.

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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
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.
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