KIF18B promotes hepatocellular carcinoma progression through activating Wnt/β‐catenin‐signaling pathway
| العنوان: | KIF18B promotes hepatocellular carcinoma progression through activating Wnt/β‐catenin‐signaling pathway |
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| المؤلفون: | Chunping Wang, Yihui Rong, Bin Yang, Yin-Ying Lu, Shengzhi Wang, Zhenwen Liu, Xudong Gao, Hui Xie |
| المصدر: | Journal of Cellular Physiology. 235:6507-6514 |
| بيانات النشر: | Wiley, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, Carcinoma, Hepatocellular, Physiology, Clinical Biochemistry, Clone (cell biology), Kinesins, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Western blot, Cell Movement, Cell Line, Tumor, medicine, Humans, Wnt Signaling Pathway, beta Catenin, Cell Proliferation, Gene knockdown, Messenger RNA, Oncogene, medicine.diagnostic_test, Chemistry, Liver Neoplasms, Wnt signaling pathway, Hep G2 Cells, Cell Biology, Middle Aged, digestive system diseases, Up-Regulation, Gene Expression Regulation, Neoplastic, 030104 developmental biology, 030220 oncology & carcinogenesis, Disease Progression, Cancer research, Immunohistochemistry, Female |
| الوصف: | This study aimed to investigate the functional roles of kinesin family member 18B (KIF18B) in hepatocellular carcinoma (HCC) development, as well as the related molecular mechanisms. Tissue specimens were collected from 105 patients with HCC, and the messenger RNA (mRNA) and protein levels of KIF18B were detected using quantitative real-time polymerase chain reaction and immunohistochemistry assays, respectively. The χ2 test was performed to estimate the association of KIF18B with clinical characteristics of patients with HCC. Effects of KIF18B expression on biological behaviors of HCC cells were detected by clone formation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and transwell assays. The expression patterns of proteins were investigated using Western blot analysis. HCC tissues and cell lines showed significant upregulation of KIF18B at both mRNA and protein levels (p > .05, for all). Furthermore, the elevated KIF18B expression was positively correlated with the tumor-node-metastasis stage (p = .015) and lymph node metastasis (p = .007). Knockdown of KIF18B might suppress HCC cell clone formation, proliferation, migration, and invasion in vitro. Besides, the activity of Wnt/β-catenin pathway was also significantly inhibited after the KIF18B knockdown. However, the antitumor actions caused by KIF18B knockdown might be reversed by lithium chloride treatment, which was the inducer of Wnt/β-catenin-signaling pathway. KIF18B may serve as an oncogene in HCC through enhancing the activity of Wnt/β-catenin pathway. |
| تدمد: | 1097-4652 0021-9541 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::99917f8e62be3cc8f6420af3effb44f4 https://doi.org/10.1002/jcp.29444 |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi.dedup.....99917f8e62be3cc8f6420af3effb44f4 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10974652 00219541 |
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