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长链非编码RNA EGOT在结肠癌中的表达及其对结肠癌细胞自噬的影响的临床意义研究

Study on Clinical Significance of LncRNA EGOT Expression in Colon Cancer and Its Effect on Autophagy of Colon Cancer Cells.

作者信息

Liu Yang, Zhang Bo, Cao Wen-Bin, Wang Hai-Yan, Niu Lei, Zhang Guo-Zhi

机构信息

Department of General Surgery, North China University of Science and Technology Affiliated Hospital, Tangshan City, Hebei Province 063000, People's Republic of China.

Department of Oncology, The 982 Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Tangshan City, Hebei Province 063000, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Dec 31;12:13501-13512. doi: 10.2147/CMAR.S285254. eCollection 2020.

DOI:10.2147/CMAR.S285254
PMID:33408522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7781029/
Abstract

BACKGROUND

Colon cancer (CC) is a common digestive tract tumor, and the increase of new and dead patients every year still puzzles clinical workers. LncRNA eosinophil granule ontogeny transcript (), as a newly discovered long-chain noncoding RNA (lncRNA), is differentially expressed in other tumors, but there are fewer studies of it in colon cancer.

METHODS

The relative expression and diagnostic value of in CC were detected and analyzed by starBase online website and qRT-PCR. The patients were followed-up for five years, and Cox regression was used to analyze the independent prognostic factors of CC. The effects of overexpression (pcDNA-RGOT) on CC cell function were detected by CCK-8, transwell and flow cytometry. WB was applied to detect autophagy. The influence of knocking out (sh-) on tumor growth was observed by tumor allogeneic inhibition. The microRNA (miR) and mRNA in the downstream of were predicted and the ceRNA network map was drawn.

RESULTS

The online database and qRT-PCR detection showed that was highly expression in patients with CC and had good diagnostic value. The five-year survival rate of patients with high expression of decreased. and TNM staging were independent prognostic factors of patients with CC. Functional analysis revealed that the growth and invasion abilities of cells increased, and the apoptosis rate decreased after overexpression. Upregulation of inhibited autophagy of CC cells and promoted cell growth. However, the tumor in nude mice was significantly lessened after knockout of . Bioinformatic analysis showed that microRNA-33a-5p and microRNA-33b-5p had targeted binding sites with .

CONCLUSION

is highly expressed in CC and has high diagnostic value. In addition, inhibition of can promote autophagy of CC cells and inhibit cell growth and metastasis, which is expected to be a potential therapeutic index.

摘要

背景

结肠癌(CC)是一种常见的消化道肿瘤,每年新增和死亡患者数量的增加仍困扰着临床工作者。长链非编码RNA嗜酸性粒细胞颗粒发生转录本(),作为新发现的长链非编码RNA(lncRNA),在其他肿瘤中存在差异表达,但在结肠癌中的研究较少。

方法

通过starBase在线网站和qRT-PCR检测并分析CC中 的相对表达及诊断价值。对患者进行五年随访,采用Cox回归分析CC的独立预后因素。通过CCK-8、transwell和流式细胞术检测过表达(pcDNA-RGOT)对CC细胞功能的影响。应用WB检测自噬。通过肿瘤异体抑制观察敲除 (sh-)对肿瘤生长的影响。预测 下游的微小RNA(miR)和mRNA,并绘制ceRNA网络图。

结果

在线数据库和qRT-PCR检测显示, 在CC患者中高表达且具有良好的诊断价值。 高表达患者的五年生存率降低。 和TNM分期是CC患者的独立预后因素。功能分析显示,过表达后细胞的生长和侵袭能力增强,凋亡率降低。 的上调抑制了CC细胞的自噬并促进细胞生长。然而,敲除 后裸鼠体内的肿瘤明显减小。生物信息学分析表明,微小RNA-33a-5p和微小RNA-33b-5p与 具有靶向结合位点。

结论

在CC中高表达且具有较高的诊断价值。此外,抑制 可促进CC细胞的自噬并抑制细胞生长和转移,有望成为潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/87a97d85c009/CMAR-12-13501-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/16a17a5c1707/CMAR-12-13501-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/61dbec94748d/CMAR-12-13501-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/bf86a1fa008c/CMAR-12-13501-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/eb851b762398/CMAR-12-13501-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/a16f9952e2ae/CMAR-12-13501-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/87a97d85c009/CMAR-12-13501-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/16a17a5c1707/CMAR-12-13501-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/61dbec94748d/CMAR-12-13501-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/bf86a1fa008c/CMAR-12-13501-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/eb851b762398/CMAR-12-13501-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/a16f9952e2ae/CMAR-12-13501-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09de/7781029/87a97d85c009/CMAR-12-13501-g0006.jpg

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