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长链非编码 RNA 重编程调控因子通过表皮生长因子受体信号通路在结肠癌进展中的作用。

Role of Long Noncoding RNA Regulator of Reprogramming in Colon Cancer Progression via Epidermal Growth Factor Receptor Signaling.

机构信息

Department of Oncology, 117932Nantong City No. 1 People's Hospital and Second Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.

Research Center of Clinical Medicine, 74567The Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.

出版信息

Technol Cancer Res Treat. 2022 Jan-Dec;21:15330338221114707. doi: 10.1177/15330338221114707.

DOI:10.1177/15330338221114707
PMID:35946134
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9373180/
Abstract

Long intergenic noncoding RNA regulator of reprogramming (linc-ROR) is a novel long noncoding RNA that exhibits significant effects on cancer progression. This research presented that linc-ROR had a crucial part in promoting biological characteristics associated with worse prognosis in colon cancer. Bioinformatics analysis was performed to predict signaling pathways related to linc-ROR. In addition, western blot, quantitative reverse transcription-polymerase chain reaction, RNA-pulldown, cell proliferation assays, colony formation assays, wound healing assays, and transwell assays were applied to detect the role and regulation of particular molecules. Our results showed that the knockdown of linc-ROR reduced cell invasion, proliferative ability, and migration in colon cancer. Further evaluation verified that downregulating linc-ROR inhibited the activation of epidermal growth factor receptor (EGFR) signaling. In addition, cbl-b, a kind of E3 ubiquitin ligase that increases the degradation of EGFR, was found to be a potential linc-ROR target. Based on our findings, it was presented that linc-ROR served a role as a tumor-promoting factor via repressing the ubiquitination and degradation of EGFR signaling, which indicated that it could be a possible prognostic marker and therapeutic target for colon cancer.

摘要

长链非编码 RNA 调控重编程(linc-ROR)是一种新型长链非编码 RNA,对癌症进展有显著影响。本研究表明,linc-ROR 在促进与结直肠癌预后不良相关的生物学特征方面起着关键作用。进行了生物信息学分析以预测与 linc-ROR 相关的信号通路。此外,还应用了 Western blot、定量逆转录聚合酶链反应、RNA 下拉、细胞增殖测定、集落形成测定、划痕愈合测定和 Transwell 测定来检测特定分子的作用和调节。我们的结果表明,linc-ROR 的敲低降低了结肠癌的侵袭、增殖能力和迁移。进一步评估证实,下调 linc-ROR 抑制了表皮生长因子受体(EGFR)信号的激活。此外,cbl-b,一种增加 EGFR 降解的 E3 泛素连接酶,被发现是 linc-ROR 的潜在靶标。基于我们的发现,提出 linc-ROR 通过抑制 EGFR 信号的泛素化和降解来充当肿瘤促进因子,这表明它可能是结直肠癌的一个潜在预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/2e28468a8b5e/10.1177_15330338221114707-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/cd8472856bad/10.1177_15330338221114707-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/24e1e00d77ca/10.1177_15330338221114707-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/51810e46e8d1/10.1177_15330338221114707-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/be643e87cf3e/10.1177_15330338221114707-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/1c284ac03cef/10.1177_15330338221114707-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/6dd0752b1324/10.1177_15330338221114707-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/5d8c38cd5d71/10.1177_15330338221114707-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/2e28468a8b5e/10.1177_15330338221114707-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/cd8472856bad/10.1177_15330338221114707-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/24e1e00d77ca/10.1177_15330338221114707-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/51810e46e8d1/10.1177_15330338221114707-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/be643e87cf3e/10.1177_15330338221114707-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/1c284ac03cef/10.1177_15330338221114707-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/6dd0752b1324/10.1177_15330338221114707-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/5d8c38cd5d71/10.1177_15330338221114707-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffc6/9373180/2e28468a8b5e/10.1177_15330338221114707-fig8.jpg

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本文引用的文献

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