SNHG17 , as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma
| العنوان: | SNHG17 , as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma |
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| المؤلفون: | Xiaoliang Liang, Yanli Guo, Zhiming Dong, Bo Feng, Gaoyan Wang, Supeng Shen, Jia Liang, Wei Guo |
| المصدر: | Cancer Science |
| بيانات النشر: | Wiley, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Genetics, Genomics and Proteomics, Male, Cancer Research, Epithelial-Mesenchymal Transition, Esophageal Neoplasms, Proto-Oncogene Proteins c-jun, Proto-Oncogene Proteins c-myc, Mice, Downregulation and upregulation, Cell Movement, Transcription (biology), Cell Line, Tumor, metastasis, Animals, Humans, PI3K/AKT/mTOR pathway, Cell Proliferation, Neoplasm Staging, Chemistry, c-jun, EMT, RNA, Promoter, Original Articles, General Medicine, Long non-coding RNA, esophageal squamous cell carcinoma, SNHG17, Up-Regulation, Gene Expression Regulation, Neoplastic, Oncology, c‐Myc, Cancer research, Original Article, Female, RNA, Long Noncoding, Chromatin immunoprecipitation, Neoplasm Transplantation |
| الوصف: | Dysregulation of long noncoding RNA SNHG17 is associated with the occurrence of several tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains obscure. The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF‐β1, and associated with poor survival. It is also involved in the epithelial‐to‐mesenchymal transition (EMT) process. The mechanism underlying SNHG17‐regulated c‐Myc was detected by RNA immunoprecipitation, RNA pull‐down, chromatin immunoprecipitation, and luciferase reporter assays. SNHG17 was found to directly regulate c‐Myc transcription by binding to c‐Jun protein and recruiting the complex to specific sequences of the c‐Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF‐β1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. Overall, this study demonstrated that the SNHG17/c‐Jun/c‐Myc axis aggravates ESCC progression and EMT induction by TGF‐β1 and may serve as a new therapeutic target for ESCC. SNHG17 was upregulated and associated with poor survival in ESCC. TGF‐β1 induced SNHG17 involved in the epithelial‐to‐mesenchymal transition process and activated the PI3K/AKT pathway. Mechanistically, SNHG17 was found to directly regulate c‐Myc transcription by binding to c‐Jun protein and recruiting the complex to specific sequences of the c‐Myc promoter region. SNHG17 aggravated ESCC growth in vivo. |
| تدمد: | 1349-7006 1347-9032 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a7d8e3bd349447cd0001be2afe30024cTest https://doi.org/10.1111/cas.15184Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....a7d8e3bd349447cd0001be2afe30024c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13497006 13479032 |
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