Lncrna FEZf1-as1 negatively regulates ETNK1 to promote malignant progression of renal cell carcinoma.

IF 2 4区医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Medical Biochemistry Pub Date : 2023-03-15 DOI:10.5937/jomb0-39710

Jiangyong Lou, Xiaoming Liu, Xiaodong Fan, Xiaoming Xu, Zhichao Wang, Liqun Wang

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Abstract

Background: To explore the role of LncFEZF1-AS1 in renal cell carcinoma (RCC) tissues and cells, and the possible molecular mechanism.

Methods: Expressions of LncFEZF1-AS1 in RCC tissues and adjacent ones were detected. The association of LncFEZF1-AS1 level with clinical data of RCC patients was also analyzed. Besides, the differential expressions of LncFEZF1-AS1 in a variety of RCC cell lines were also determined. Then the LncFEZF1-AS1 knockdown model was constructed in RCC cell line to further determine the influences of LncFEZF1-AS1 on the proliferative ability and migration of RCC cells through CCK8 and Transwell experiments. Furthermore, luciferase reporter gene experiment were used to validate the combination of LncFEZF1-AS1 to ETNK1.

Results: Results suggested that expression of LncFEZF1-AS1 was noticeably higher in RCC tumor tissues and the RCC cells. Clinical pathological data analysis also suggested that high LncFEZF1-AS1 expression was in correlation with the pathological stage and the incidence of distant metastasis in RCC patients, and the poor overall survival rate. In vitro experiments demonstrated that knocking down of LncFEZF1-AS1 markedly repressed the proliferation and migration of RCC cell lines. Bioinformatics suggested that LncFEZF1-AS1 can interact with the downstream target gene ETNK1, which was confirmed by the luciferase reporter gene experiments. Western Blot results revealed that knocking down of LncFEZF1-AS1 markedly enhanced ETNK1. qRT-PCR analysis indicated that ETNK1 level was under-expressed in RCC tissues and in negative correlation with LncFEZF1-AS1. Further experiments suggested that knockdown of ETNK1 partially reversed the inhibitory effects of LncFEZF1-AS1 silencing on the proliferative and migrative abilities of RCC cells.

Conclusions: LncFEZF1-AS1 could facilitation the proliferative and migration of RCC cells by regulating the expression of ETNK1. Therefore, FEZF1-AS1 might function as a cancer-promoting factor and possible new therapeutic target for RCC.

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Lncrna FEZf1-as1负调控ETNK1促进肾细胞癌恶性进展。

背景:探讨LncFEZF1-AS1在肾细胞癌(RCC)组织和细胞中的作用及其可能的分子机制。方法:检测LncFEZF1-AS1在RCC组织及癌旁组织中的表达。分析lcfezf1 - as1水平与RCC患者临床资料的相关性。此外，我们还检测了lcfezf1 - as1在不同RCC细胞系中的表达差异。然后在RCC细胞系中构建LncFEZF1-AS1敲低模型，通过CCK8和Transwell实验进一步确定LncFEZF1-AS1对RCC细胞增殖能力和迁移能力的影响。通过荧光素酶报告基因实验验证lnfezf1 - as1与ETNK1的结合。结果:结果提示LncFEZF1-AS1在RCC肿瘤组织及细胞中的表达明显增高。临床病理资料分析也提示，LncFEZF1-AS1高表达与RCC患者的病理分期及远处转移发生率相关，且总生存率较差。体外实验表明，敲低lnfezf1 - as1可显著抑制RCC细胞株的增殖和迁移。生物信息学提示LncFEZF1-AS1可与下游靶基因ETNK1相互作用，荧光素酶报告基因实验证实了这一点。Western Blot结果显示，lnfezf1 - as1基因的敲除显著增强了ETNK1。qRT-PCR分析显示，ETNK1水平在RCC组织中低表达，且与LncFEZF1-AS1呈负相关。进一步的实验表明，敲低ETNK1部分逆转了LncFEZF1-AS1沉默对RCC细胞增殖和迁移能力的抑制作用。结论:lcfezf1 - as1可通过调节ETNK1的表达促进RCC细胞的增殖和迁移。因此，FEZF1-AS1可能是一种促癌因子，可能是RCC新的治疗靶点。

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 Medical Biochemistry BIOCHEMISTRY & MOLECULAR BIOLOGY-

CiteScore

3.00

自引率

12.00%

发文量

审稿时长

>12 weeks

期刊介绍： The JOURNAL OF MEDICAL BIOCHEMISTRY (J MED BIOCHEM) is the official journal of the Society of Medical Biochemists of Serbia with international peer-review. Papers are independently reviewed by at least two reviewers selected by the Editors as Blind Peer Reviews. The Journal of Medical Biochemistry is published quarterly. The Journal publishes original scientific and specialized articles on all aspects of clinical and medical biochemistry, molecular medicine, clinical hematology and coagulation, clinical immunology and autoimmunity, clinical microbiology, virology, clinical genomics and molecular biology, genetic epidemiology, drug measurement, evaluation of diagnostic markers, new reagents and laboratory equipment, reference materials and methods, reference values, laboratory organization, automation, quality control, clinical metrology, all related scientific disciplines where chemistry, biochemistry, molecular biology and immunochemistry deal with the study of normal and pathologic processes in human beings.