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lncRNA 00312 通过 miR-34a-5p/ASS1 轴抑制肾细胞癌的细胞增殖、侵袭并促进凋亡。

lncRNA 00312 Attenuates Cell Proliferation and Invasion and Promotes Apoptosis in Renal Cell Carcinoma via miR-34a-5p/ASS1 Axis.

机构信息

Department of Clinical Laboratory, Mianyang Central Hospital, Affiliated to Southwest Medical University, Mianyang 621000, Sichuan Province, China.

Department of Medical Laboratory, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China.

出版信息

Oxid Med Cell Longev. 2020 Mar 23;2020:5737289. doi: 10.1155/2020/5737289. eCollection 2020.

DOI:10.1155/2020/5737289
PMID:32308805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7140129/
Abstract

BACKGROUND

Previous studies have demonstrated that lncRNAs play functional roles in regulating cancer cell proliferation, invasion, and apoptosis. Recent studies confirmed that lncRNA 00312 has important biological functions in lung and colorectal cancer. However, the role of lncRNA 00312 in renal cell carcinoma (RCC) remains unclear. Our aim was to explore the function of lncRNA 00312 in RCC and its potential molecular mechanism.

METHODS

RCC cell lines A498 and ACHN were used as models in this study. RT-PCR was performed to determine lncRNA 00312, miR-34a-5p, and ASS1 mRNA expression. Proliferation and invasion were examined by CCK-8 and Transwell assay to confirm the function role of lncRNA 00312. Western blot analysis was used to examine the expression of apoptotic proteins Bax and Bcl-2.

RESULTS

lncRNA was significantly downregulated in RCC cells such as A498 and ACHN; the expression of lncRNA 00312 in RCC tissues was significantly lower than that in adjacent normal tissues. Patients with low expression of lncRNA 00312 have worse prognosis regarding pathological grade, tumor size, and TNM stage. Overexpression of lncRNA 00312 suppressed A498 and ACHN cell proliferation and invasion, while promoting apoptosis. Our study found that miR-34a-5p had the potential binding site with lncRNA 00312 and revealed the role of miR-34a-5p in RCC. Furthermore, we confirmed that lncRNA 00312 played its role with the participation of ASS1 and miR-34a-5p.

CONCLUSION

lncRNA 00312 can inhibit RCC proliferation and invasion and promote apoptosis by suppressing miR-34a-5p and overexpressing ASS1. Our study demonstrated that the lncRNA 00312/miR-34a-5p/ASS1 axis may play a functional role in the progression of RCC; lncRNA 00312 abundance is a prognostic factor candidate for RCC survival, which provides new insights for RCC clinical treatment. models in this study. RT-PCR was performed to determine lncRNA 00312, miR-34a-5p, and ASS1 mRNA expression. Proliferation and invasion were examined by CCK-8 and Transwell assay to confirm the function role of lncRNA 00312. Western blot analysis was used to examine the expression of apoptotic proteins Bax and Bcl-2.

摘要

背景

先前的研究表明,lncRNAs 在调节癌细胞增殖、侵袭和凋亡方面发挥着功能作用。最近的研究证实,lncRNA 00312 在肺癌和结直肠癌中具有重要的生物学功能。然而,lncRNA 00312 在肾细胞癌(RCC)中的作用尚不清楚。我们的目的是探讨 lncRNA 00312 在 RCC 中的功能及其潜在的分子机制。

方法

本研究采用 RCC 细胞系 A498 和 ACHN 作为模型。通过 RT-PCR 测定 lncRNA 00312、miR-34a-5p 和 ASS1 mRNA 的表达。通过 CCK-8 和 Transwell 测定来检测 lncRNA 00312 的增殖和侵袭功能。Western blot 分析用于检测凋亡蛋白 Bax 和 Bcl-2 的表达。

结果

lncRNA 在 RCC 细胞(如 A498 和 ACHN)中显著下调;RCC 组织中 lncRNA 00312 的表达明显低于邻近正常组织。lncRNA 00312 低表达的患者在病理分级、肿瘤大小和 TNM 分期方面预后较差。过表达 lncRNA 00312 可抑制 A498 和 ACHN 细胞的增殖和侵袭,同时促进细胞凋亡。我们的研究发现,miR-34a-5p 与 lncRNA 00312 具有潜在的结合位点,并揭示了 miR-34a-5p 在 RCC 中的作用。此外,我们证实 lncRNA 00312 通过 ASS1 和 miR-34a-5p 的参与发挥其作用。

结论

lncRNA 00312 通过抑制 miR-34a-5p 和过表达 ASS1 抑制 RCC 增殖和侵袭,促进细胞凋亡。本研究表明,lncRNA 00312/miR-34a-5p/ASS1 轴可能在 RCC 进展中发挥功能作用;lncRNA 00312 的丰度是 RCC 生存的候选预后因素,为 RCC 的临床治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/91dc1a9d968f/OMCL2020-5737289.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/95aee872f1e4/OMCL2020-5737289.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/b2ec0a424381/OMCL2020-5737289.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/be3a7cc05188/OMCL2020-5737289.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/eeb0c4d5661a/OMCL2020-5737289.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/c41342f0276f/OMCL2020-5737289.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/91dc1a9d968f/OMCL2020-5737289.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/95aee872f1e4/OMCL2020-5737289.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/b2ec0a424381/OMCL2020-5737289.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/be3a7cc05188/OMCL2020-5737289.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/eeb0c4d5661a/OMCL2020-5737289.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/c41342f0276f/OMCL2020-5737289.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/782b/7140129/91dc1a9d968f/OMCL2020-5737289.006.jpg

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