CKS1B promotes cell proliferation and invasion by activating STAT3/PD‐L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma

التفاصيل البيبلوغرافية
العنوان: CKS1B promotes cell proliferation and invasion by activating STAT3/PD‐L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma
المؤلفون: Hui Wang, Zhe Yan, Zhengdong Zhang, Shihong Ma
المصدر: Journal of Clinical Laboratory Analysis
بيانات النشر: Wiley, 2020.
سنة النشر: 2020
مصطلحات موضوعية: STAT3 Transcription Factor, 0301 basic medicine, Microbiology (medical), endocrine system diseases, Clinical Biochemistry, B7-H1 Antigen, 03 medical and health sciences, 0302 clinical medicine, Cell Line, Tumor, CDC2-CDC28 Kinases, Humans, Immunology and Allergy, Neoplasm Invasiveness, Thyroid Neoplasms, Viability assay, Phosphorylation, STAT3, Protein kinase B, Research Articles, Cell Proliferation, STAT3/PD‐L1, Gene knockdown, biology, Cell growth, Chemistry, Akt, Biochemistry (medical), Public Health, Environmental and Occupational Health, Hematology, Transfection, Gene Expression Regulation, Neoplastic, Medical Laboratory Technology, CKS1B, 030104 developmental biology, Thyroid Cancer, Papillary, Cell culture, 030220 oncology & carcinogenesis, papillary thyroid carcinoma, Cancer research, biology.protein, Signal Transduction, Research Article
الوصف: Objective To investigate role of GKS1B and its relationship between STAT3/PD‐L1 and p‐Akt in papillary thyroid carcinoma (PTC). Methods Expression of GKS1B and PD‐L1 was determined in PTC cell lines. GKS1B was overexpressed or knocked down by transfection with overexpression plasmids or si‐CKS1B. STAT3 inhibitor WP1066 was used to suppress STAT3, and PD‐L1 inhibitor Pembrolizumab was used to block PD‐L1. Cell viability and invasion were evaluated by MTT and transwell assay, respectively. The expression of STAT3, p‐STAT3, Akt, and p‐Akt was measured using Western blotting. Results Both protein levels and mRNA levels of CKS1B and PD‐L1 were remarkably up‐regulated in PTC cell lines. Knockdown of CKS1B significantly inhibited cell viability and invasion of PTC cells and suppressed STAT3/PD‐L1 signaling and Akt phosphorylation, while overexpression of CKS1B led to opposite results. Inhibition of STAT3 or PD‐L1 reversed the effects of overexpressed CKS1B on PTC cells. Conclusion The overexpression of CSK1B could promote cell viability and invasion of PTC cells through activation of STAT3/PD‐L1 signaling and Akt phosphorylation.
In the present study, we demonstrated that the overexpression of CSK1B could promote cell viability and invasion of PTC cells through activation of STAT3/PD‐L1 signaling and Akt phosphorylation. This study might provide deeper understanding of CSK1B/STAT3/PD‐L1 axis in PTC development.
تدمد: 1098-2825
0887-8013
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9221ed7a28ef500d0464c99cdd99cae4
https://doi.org/10.1002/jcla.23565
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....9221ed7a28ef500d0464c99cdd99cae4
قاعدة البيانات: OpenAIRE