LncRNA FAM83A‐AS1 promotes lung adenocarcinoma progression by enhancing the pre‐mRNA stability of FAM83A
| العنوان: | |
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| المؤلفون: | Zhunlin Zhao, Jun Chen, Chang Li, Jun Zhao, Tengfei Chen, Chun Xu, Cheng Ding, Wen-Yi Wang |
| المصدر: | Thoracic Cancer Thoracic Cancer, Vol 12, Iss 10, Pp 1495-1502 (2021) |
| بيانات النشر: | Wiley, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | LUAD, 0301 basic medicine, Pulmonary and Respiratory Medicine, Lung Neoplasms, Adenocarcinoma of Lung, Transfection, medicine.disease_cause, 03 medical and health sciences, lncRNA, 0302 clinical medicine, Humans, Medicine, FAM83A‐AS1, RC254-282, Messenger RNA, Gene knockdown, Oncogene, business.industry, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RNA, Cancer, Nuclease protection assay, Original Articles, General Medicine, medicine.disease, Neoplasm Proteins, Antisense RNA, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Disease Progression, Cancer research, Original Article, RNA, Long Noncoding, business, Carcinogenesis, FAM83A |
| الوصف: | Background Lung cancer is the leading cause of cancer deaths worldwide. Long non‐coding RNAs (lncRNAs) affect a series of cellular biological processes, including oncogene function promotion. In this study, we explored the functions and mechanisms of FAM83A antisense RNA 1 (FAM83A‐AS1) in non‐small cell lung cancer (NSCLC) progression. Methods The expression of FAM83A‐AS1and FAM83A mRNA was analyzed using the Cancer Genome Atlas (TCGA) data. Proliferation, migration, invasion and Western blotting were measured after treatment with overexpressed or knockdown FAM83A‐AS1. To determine the relationship between FAM83A‐AS1 and FAM83A, RNase protection assay (RPA), amanitin treatment, RNA pulldown assay and RNA immunoprecipitation (RIP) assay were performed. Results High expression of FAM83A‐AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression‐free survival (PFS). Functionally, high FAM83A‐AS1 expression increased LUAD cell proliferation and metastasis, indicating that FAM83A‐AS1 exerted its oncogenic functions. Furthermore, FAM83A‐AS1 promoted NSCLC progression via ERK signaling pathways. Mechanistically, FAM83A‐AS1 post‐transcriptionally increased FAM83A expression by enhancing pre‐mRNA stability. FAM83A‐AS1 enhanced FAM83A mRNA stability not only by forming an RNA duplex but also by binding to FBL. Conclusions We determined that FAM83A‐AS1 increased FAM83A expression by enhancing FAM83A pre‐mRNA stability and promoted the tumorigenesis of LUAD. High expression of FAM83A‐AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression‐free survival (PFS). FAM83A‐AS1 increased FAM83A expression by enhancing FAM83A pre‐mRNA stability and promoted the tumorigenesis of LUAD. |
| تدمد: | 1759-7714 1759-7706 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ad2dd653631ea99b9604639c352581fcTest https://doi.org/10.1111/1759-7714.13928Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....ad2dd653631ea99b9604639c352581fc |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17597714 17597706 |
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