CUL4A regulates endometrial cancer cell proliferation, invasion and migration by interacting with CSN6

التفاصيل البيبلوغرافية
العنوان: CUL4A regulates endometrial cancer cell proliferation, invasion and migration by interacting with CSN6
المؤلفون: Tianquan Chen, Xiangrong Wang
المصدر: Molecular Medicine Reports
بيانات النشر: D.A. Spandidos, 2020.
سنة النشر: 2020
مصطلحات موضوعية: 0301 basic medicine, Cancer Research, Epithelial-Mesenchymal Transition, proliferation, Cell, migration, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Cell Line, Tumor, Genetics, medicine, Humans, Neoplasm Invasiveness, Protein Interaction Maps, Molecular Biology, Adaptor Proteins, Signal Transducing, Cell Proliferation, Gene knockdown, Oncogene, Cell growth, Chemistry, COP9 Signalosome Complex, Sequence Analysis, RNA, Gene Expression Profiling, Transfection, Articles, Cell cycle, invasion, Cullin Proteins, Molecular biology, Endometrial Neoplasms, Up-Regulation, Blot, Gene Expression Regulation, Neoplastic, 030104 developmental biology, medicine.anatomical_structure, Oncology, Matrix Metalloproteinase 9, Apoptosis, 030220 oncology & carcinogenesis, endometrial cancer, cullin 4A, Molecular Medicine, Matrix Metalloproteinase 2, Female, Tumor Suppressor Protein p53
الوصف: Endometrial cancer (EC) is a common malignant gynecological tumor arising from the endometrium, with an annually increasing morbidity and mortality. The present study aimed to investigate the functions of cullin 4A (CUL4A) in EC, as well as the underlying mechanisms. CUL4A expression was assessed in several human EC cells and normal human endometrial epithelial cells (hEECs) via reverse transcription‑quantitative polymerase chain reaction and western blotting. Subsequently, short hairpin (sh)RNA‑CULA4 was transfected into cells, and cell proliferation, invasion and migration were detected using Cell Counting kit‑8, Transwell and wound healing assays, respectively. The STRING database identified that CSN6 interacted with CULA4, and immunoprecipitation was performed to verify the interaction. Subsequently, following CUL4A knockdown, pcDNA3.1‑CSN6 was transfected into cells and its effects on cell proliferation, invasion and migration were assessed. The expression levels of matrix metallopeptidase (MMP)2, MMP9 and p53 were evaluated via western blotting. The results indicated that CUL4A was highly expressed in EC cells, compared with hEECs. CULA4‑knockdown notably inhibited EC cell proliferation, invasion and migration. The expression levels of MMP2 and MMP9 were significantly decreased, while p53 expression was enhanced following CUL4A‑knockdown. The immunoprecipitation assay verified that COP9 signalosome subunit 6 (CSN6) interacted with CULA4. Furthermore, CSN6‑overexpression alleviated the inhibitory effects of CUL4A‑knockdown on EC cell proliferation, invasion and migration. Similarly, CSN6 overexpression reversed CUL4A‑knockdown‑mediated effects on the expression of MMP2, MMP9 and p53. In summary, the results demonstrated that CUL4A regulated EC cell proliferation, invasion and migration by interacting with CSN6.
اللغة: English
تدمد: 1791-3004
1791-2997
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7aaa296736b1978728e1e49d4ba64435
http://europepmc.org/articles/PMC7673334
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....7aaa296736b1978728e1e49d4ba64435
قاعدة البيانات: OpenAIRE