Long non-coding RNA PCED1B antisense RNA 1 promotes gastric cancer progression via modulating microRNA-215-3p / C-X-C motif chemokine receptor 1 axis
العنوان: | Long non-coding RNA PCED1B antisense RNA 1 promotes gastric cancer progression via modulating microRNA-215-3p / C-X-C motif chemokine receptor 1 axis |
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المؤلفون: | Ruize Zhou, Fengchang Huang, Junyu Ren, Wenliang Li, Ning Xu, Hongbin Zhang |
المصدر: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 12, Iss 1, Pp 6083-6095 (2021) |
بيانات النشر: | Taylor & Francis, 2021. |
سنة النشر: | 2021 |
مصطلحات موضوعية: | Male, Bioengineering, Applied Microbiology and Biotechnology, Receptors, Interleukin-8A, Chemokine receptor, Stomach Neoplasms, Cell Line, Tumor, microRNA, Humans, Gene, GC, Reporter gene, CXCR1, Chemistry, Cell growth, RNA, General Medicine, Middle Aged, Long non-coding RNA, Antisense RNA, MicroRNAs, Cancer research, Female, RNA, Long Noncoding, PCED1B-AS1, miR-215-3p, TP248.13-248.65, Biotechnology, Research Article, Research Paper |
الوصف: | Long non-coding RNAs (lncRNAs) emerge as vital modulators and tissue-specific biomarkers of multiple cancers, including gastric cancer (GC). Instead, the expression characteristics, biological function and molecular mechanism of lncRNA PCED1B antisense RNA 1 (PCED1B-AS1) in GC await more elaboration. In this study, 48 cases of GC tissues and matched non-cancerous tissues were collected, and PCED1B-AS1, microRNA-215-3p (miR-215-3p) and C-X-C motif chemokine receptor 1 (CXCR1) expression levels were detected by qRT-PCR. Besides, CCK-8, EdU, Transwell and Western blot assays were conducted to assess the impact of PCED1B-AS1 or miR-215-3p on cell growth, migration, invasion and epithelial-mesenchymal transition (EMT). The interaction between genes was verified by bioinformatics analysis, rna immunoprecitipation (RIP) and dual-luciferase reporter gene assays. We demonstrated that, PCED1B-AS1 expression level was raised in GC tissues and cell lines, and increased expression of PCED1B-AS1 was in association with tumor size, TNM stage and lymph node metastasis in GC patients. Additionally, PCED1B-AS1 overexpression promoted GC cells proliferation, migration, invasion and EMT, and miR-215-3p overexpression counteracted the biological effects of PCED1B-AS1. Mechanistically, PCED1B-AS1 specifically inhibited miR-215-3p expressions, thus up-regulating CXCR1 expressions. In conclusion, PCED1B-AS1 accelerates GC progression via adsorbing miR-215-3p and up-regulating CXCR1, indicating that PCED1B-AS1 is a novel therapeutic target for treating GC. |
اللغة: | English |
تدمد: | 2165-5987 2165-5979 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6ad3f6016ff8a3e7586ccc1b86328e89Test http://europepmc.org/articles/PMC8806612Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....6ad3f6016ff8a3e7586ccc1b86328e89 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 21655987 21655979 |
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