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长链非编码RNA U731166通过在食管鳞状细胞癌(ESCC)中吸附miR-3607-3p增加转化生长因子β受体1(TGFBR1)的积累,从而促进肿瘤转移。

LncRNA U731166 Increases the Accumulation of TGFBR1 by Sponging miR-3607-3p in Esophageal Squamous-Cell Carcinomas (ESCC) to Promote Tumor Metastasis.

作者信息

Wang Mingbo, Wang Meng, Huang Chao, Zhu Yonggang, Zhang Fan, Gao Wenda, Li Zhenhua, Peng Liangbiao, Tian Ziqiang, Gao Chao, Han Xingpeng

机构信息

Department of Thoracic Surgery,The Fourth Hospital of Hebei Medical University Shijiazhuang City, Hebei Province, 050000, PR. China.

Thoracic surgery Department,Tianjin Chest hospital, Tianjin City, 300222, PR. China.

出版信息

Iran J Biotechnol. 2024 Jul 1;22(3):e3391. doi: 10.30498/ijb.2024.343750.3391. eCollection 2024 Jul.

DOI:10.30498/ijb.2024.343750.3391
PMID:39737207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11682522/
Abstract

BACKGROUND

Long non-coding RNA (lncRNA) U731166 and microRNA (miR)-3607-3p are two ncRNAs with critical roles in cancer biology, while their involvement in esophageal squamous-cell carcinomas (ESCC) is unclear. We predicted that U731166 and miR-3607-3p might interact with each other. This study aimed to investigate their role and interaction in ESCC.

OBJECTIVES

This study was therefore conducted to explore the involvement of U731166 and miR-3607-3p in ESCC, with a focus on the interaction between them.

MATERIALS AND METHODS

Paired ESCC and non-tumor tissue samples were recruited from 72 ESCC patients. By RT-Qpcr, level of U731166 and miR-3607-3p in paired tissues was measured. By RNA-RNA pulldown assay, the direct interaction between U731166 and miR-3607-3p was detected. U731166 overexpression or miR-3607-3p overexpression was performed to investigate their role in regulating the expression of each other. By RT-qPCR and Western blot analysis, the role of U731166 and miR-3607-3p in regulating the level of TGFBR1 was assessed. By Transwell assays, cell invasion and migration were analyzed.

RESULTS

Compared to non-tumor tissues, U731166 was highly upregulated in ESCC, while miR-3607-3p was downregulated in ESCC. U731166 and miR-3607-3p directly interacted with each other, but they are not closely correlated and did not regulate the level of each other. Moreover, U731166 reversed the role of miR-3607-3p in downregulating TGFBR1 and inhibiting cancer cell invasion and migration. U731166 and miR-3607-3p were closely associated with patients' tumor metastasis but not tumor size.

CONCLUSION

U731166 may upregulate TGFBR1 by sponging miR-3607-3p in ESCC cells to promote tumor metastasis.

摘要

背景

长链非编码RNA(lncRNA)U731166和微小RNA(miR)-3607-3p是在癌症生物学中起关键作用的两种非编码RNA,而它们在食管鳞状细胞癌(ESCC)中的作用尚不清楚。我们预测U731166和miR-3607-3p可能相互作用。本研究旨在探讨它们在ESCC中的作用及相互作用。

目的

因此,本研究旨在探讨U731166和miR-3607-3p在ESCC中的作用,重点关注它们之间的相互作用。

材料与方法

从72例ESCC患者中收集配对的ESCC组织和非肿瘤组织样本。通过RT-Qpcr检测配对组织中U731166和miR-3607-3p的水平。通过RNA-RNA下拉试验,检测U731166和miR-3607-3p之间的直接相互作用。进行U731166过表达或miR-3607-3p过表达,以研究它们在调节彼此表达中的作用。通过RT-qPCR和蛋白质免疫印迹分析,评估U731166和miR-3607-3p在调节转化生长因子β受体1(TGFBR1)水平中的作用。通过Transwell试验,分析细胞侵袭和迁移情况。

结果

与非肿瘤组织相比,U731166在ESCC中高度上调,而miR-3607-3p在ESCC中下调。U731166和miR-3607-3p直接相互作用,但它们之间没有密切相关性,也不调节彼此的水平。此外,U731166逆转了miR-3607-3p下调TGFBR1以及抑制癌细胞侵袭和迁移的作用。U731166和miR-3607-3p与患者的肿瘤转移密切相关,但与肿瘤大小无关。

结论

在ESCC细胞中,U731166可能通过吸附miR-3607-3p上调TGFBR1,从而促进肿瘤转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/53e8f5672a41/IJB-22-e3391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/08ba3a6a4d71/IJB-22-e3391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/55b966673b14/IJB-22-e3391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/fa8773277a76/IJB-22-e3391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/53e8f5672a41/IJB-22-e3391-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/08ba3a6a4d71/IJB-22-e3391-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/55b966673b14/IJB-22-e3391-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/fa8773277a76/IJB-22-e3391-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274a/11682522/53e8f5672a41/IJB-22-e3391-g004.jpg

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