The novel non‐immunological role and underlying mechanisms of B7‐H3 in tumorigenesis
| العنوان: | The novel non‐immunological role and underlying mechanisms of B7‐H3 in tumorigenesis |
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| المؤلفون: | Yi Xin Zeng, Xiangqi Zhou, Shuhui Ouyang, Xin Huang, Xiaohong Ai, Yun-Cheng Lv, Manbo Cai, Jianjun Li |
| المصدر: | Journal of Cellular Physiology. 234:21785-21795 |
| بيانات النشر: | Wiley, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | STAT3 Transcription Factor, 0301 basic medicine, Carcinogenesis, Physiology, Angiogenesis, Clinical Biochemistry, Matrix metalloproteinase, medicine.disease_cause, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, medicine, Humans, Protein kinase B, Caspase, Cell Proliferation, biology, Cell Biology, Gene Expression Regulation, Neoplastic, Vascular endothelial growth factor, Cell Transformation, Neoplastic, 030104 developmental biology, chemistry, Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Janus kinase, Reprogramming |
| الوصف: | B7 homolog 3 (B7-H3) has been proven to be involved in tumorigenesis. An elucidation of its role and underlying mechanisms is essential to an understanding of tumorigenesis and the development of effective clinical applications. B7-H3 is abnormally overexpressed in many types of cancer and is generally associated with a poor clinical prognosis. B7-H3 inhibits the initiation of the "caspase cascade" by the Janus kinase/signal transducers and activators of transcription pathway to resist tumor cell apoptosis. B7-H3 accelerates malignant proliferation by attacking the checkpoint mechanism of the tumor cell cycle through the phosphatidylinositol 3-kinase and protein kinase B pathway. B7-H3 reprograms the metabolism of glucose and lipids and transforms the metabolic flux of tumor cells to promote tumorigenesis. B7-H3 induces abnormal angiogenesis by recruiting vascular endothelial growth factor and matrix metalloproteinase to tumor lesions. B7-H3 strongly promotes tumorigenesis through antiapoptotic, pro-proliferation, metabolism reprogramming, and pro-angiogenesis. |
| تدمد: | 1097-4652 0021-9541 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5338942ea68335f65342e574f2dd886f https://doi.org/10.1002/jcp.28936 |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi.dedup.....5338942ea68335f65342e574f2dd886f |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10974652 00219541 |
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