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LINC00239 Interacts with C-Myc Promoter-Binding Protein-1 (MBP-1) to Promote Expression of C-Myc in Esophageal Squamous Cell Carcinoma
Molecular Cancer Research ( IF 4.1 ) Pub Date : 2021-09-01 , DOI: 10.1158/1541-7786.mcr-20-1025
Xiaoliang Liang 1 , Juntao Lu 1 , Zheng Wu 1 , Yanli Guo 1 , Supeng Shen 1 , Jia Liang 1 , Zhiming Dong 1 , Wei Guo 1
Affiliation  

Increasing evidence demonstrates that long non-coding RNAs (lncRNA) play a vital role in the progression of tumors, containing esophageal squamous cell carcinoma (ESCC). LINC00239 was reported as an oncogene in diverse kinds of cancers, whereas its specific role is still unclear in ESCC. In this study, we detected the expression and functional role of LINC00239 in ESCC specimens and cells, and investigated the molecular mechanisms of it. LINC00239 was highly expressed in ESCC tissues and cells, and was related to poor prognosis of patients with ESCC. The proliferation, metastasis, and invasion ability as well as epithelial–mesenchymal transition (EMT) process were all enhanced in LINC00239-overexpressed ESCC cells. LINC00239 was upregulated in TGF-β1–treated ESCC cells. Furthermore, LINC00239 was found to bind directly to the transcription factor c-Myc promoter–binding protein-1 (MBP-1). MBP-1 was detected to inhibit the transcription of c-Myc in ESCC. Moreover, LINC00239 could activate c-Myc transcription through influencing MBP-1–binding ability to c-Myc promoter. These data suggest that LINC00239 may act as an oncogene to promote the transcription of c-Myc by competitively combining with MBP-1 in ESCC, and may serve as a potential target for antitumor therapy in ESCC. Implications: LINC00239 may function as an oncogenic lncRNA in ESCC through the LINC00239/MBP-1/c-Myc axis to activate EMT process. This article is featured in Highlights of This Issue, [p. 1439][1] [1]: /lookup/volpage/19/1439?iss=9

中文翻译:

LINC00239 与 C-Myc 启动子结合蛋白-1 (MBP-1) 相互作用以促进 C-Myc 在食管鳞状细胞癌中的表达

越来越多的证据表明,长链非编码 RNA (lncRNA) 在包括食管鳞状细胞癌 (ESCC) 在内的肿瘤进展中发挥着至关重要的作用。LINC00239 被报道为多种癌症中的致癌基因,而其在 ESCC 中的具体作用仍不清楚。在这项研究中,我们检测了LINC00239在ESCC标本和细胞中的表达和功能作用,并研究了它的分子机制。LINC00239在ESCC组织和细胞中高表达,与ESCC患者预后不良有关。在 LINC00239 过表达的 ESCC 细胞中,增殖、转移和侵袭能力以及上皮间质转化 (EMT) 过程均得到增强。LINC00239 在 TGF-β1 处理的 ESCC 细胞中上调。此外,发现 LINC00239 直接与转录因子 c-Myc 启动子结合蛋白-1 (MBP-1) 结合。检测到MBP-1抑制ESCC中c-Myc的转录。此外,LINC00239 可以通过影响 MBP-1 与 c-Myc 启动子的结合能力来激活 c-Myc 转录。这些数据表明LINC00239可能作为癌基因通过与ESCC中的MBP-1竞争性结合促进c-Myc的转录,并可能作为ESCC抗肿瘤治疗的潜在靶点。启示:LINC00239 可能通过 LINC00239/MBP-1/c-Myc 轴在 ESCC 中作为致癌 lncRNA 发挥作用,以激活 EMT 过程。这篇文章被收录在本期的亮点中,[p. 1439][1][1]:/lookup/volpage/19/1439?iss=9 LINC00239 可以通过影响 MBP-1 与 c-Myc 启动子的结合能力来激活 c-Myc 转录。这些数据表明LINC00239可能作为癌基因通过与ESCC中的MBP-1竞争性结合促进c-Myc的转录,并可能作为ESCC抗肿瘤治疗的潜在靶点。启示:LINC00239 可能通过 LINC00239/MBP-1/c-Myc 轴在 ESCC 中作为致癌 lncRNA 发挥作用,以激活 EMT 过程。这篇文章被收录在本期的亮点中,[p. 1439][1][1]:/lookup/volpage/19/1439?iss=9 LINC00239 可以通过影响 MBP-1 与 c-Myc 启动子的结合能力来激活 c-Myc 转录。这些数据表明LINC00239可能作为癌基因通过与ESCC中的MBP-1竞争性结合促进c-Myc的转录,并可能作为ESCC抗肿瘤治疗的潜在靶点。启示:LINC00239 可能通过 LINC00239/MBP-1/c-Myc 轴在 ESCC 中作为致癌 lncRNA 发挥作用,以激活 EMT 过程。这篇文章被收录在本期的亮点中,[p. 1439][1][1]:/lookup/volpage/19/1439?iss=9 启示:LINC00239 可能通过 LINC00239/MBP-1/c-Myc 轴在 ESCC 中作为致癌 lncRNA 发挥作用,以激活 EMT 过程。这篇文章被收录在本期的亮点中,[p. 1439][1][1]:/lookup/volpage/19/1439?iss=9 启示:LINC00239 可能通过 LINC00239/MBP-1/c-Myc 轴在 ESCC 中作为致癌 lncRNA 发挥作用,以激活 EMT 过程。这篇文章被收录在本期的亮点中,[p. 1439][1][1]:/lookup/volpage/19/1439?iss=9
更新日期:2021-09-02
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