S100A8 facilitates cholangiocarcinoma metastasis via upregulation of VEGF through TLR4/NF‑κB pathway activation
| Autor: | Mo Chen, Ping Zheng, Mengjia Hu, Changhong Du, Junping Wang, Yu He, Shuguang Pan, Jin Zhu, Yang Xu, Peng Jiang, Jinchi Cui, Yujun Zhang, Ying Hu, Jie Bai, Jiejuan Lai |
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| Rok vydání: | 2019 |
| Předmět: |
Male
Vascular Endothelial Growth Factor A 0301 basic medicine Cancer Research Cell Apoptosis Metastasis Cholangiocarcinoma Mice chemistry.chemical_compound 0302 clinical medicine Tumor Cells Cultured Mice Inbred BALB C vascular endothelial growth factor Liver Neoplasms NF-kappa B Cell migration Articles Middle Aged Cell cycle Prognosis Gene Expression Regulation Neoplastic Survival Rate Vascular endothelial growth factor medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis cardiovascular system Female Corrigendum Signal Transduction Mice Nude Biology 03 medical and health sciences Downregulation and upregulation parasitic diseases Biomarkers Tumor medicine metastasis S100 calcium-binding protein A8 Animals Humans Calgranulin A Cell Proliferation NF-κB pathway Oncogene medicine.disease Xenograft Model Antitumor Assays Toll-Like Receptor 4 030104 developmental biology Bile Duct Neoplasms chemistry Tumor progression Cancer research Follow-Up Studies |
| Zdroj: | International Journal of Oncology |
| ISSN: | 1791-2423 1019-6439 |
| DOI: | 10.3892/ijo.2019.4907 |
| Popis: | A growing body of evidence indicates that S100 calcium‑binding protein A8 (S100A8) is frequently overexpressed in malignant tumor tissues and regulates tumor progression; however, the role of S100A8 in cholangiocarcinoma (CCA) remains unclear. The present study demonstrated that the protein expression of S100A8 was significantly higher in pathological tissues compared with adjacent normal tissues from patients with CCA. In addition, S100A8 expression was significantly associated with differentiation, lymph node metastasis and poor prognosis in patients following surgical resection of CCA. Furthermore, both in vitro and in vivo experiments revealed that overexpression of S100A8 promoted, while S100A8 knockdown attenuated, the migration and metastasis of CCA cells. Of note, the present results indicated that S100A8 promoted the CCA tumor cell‑induced migration of vascular endothelial cells. Finally, S100A8 was demonstrated to positively regulate the expression of vascular endothelial growth factor (VEGF) in CCA cells, which was mediated by activation of the Toll‑like receptor 4 (TLR4)/NF‑κB pathway. In conclusion, the present study demonstrated that S100A8 had an important role in facilitating CCA cell migration and metastasis via upregulation of VEGF expression by activating the TLR4/NF‑κB pathway. These findings may provide a novel target for CCA treatment.[the original article was published in International Journal of Oncology 56: 101‑112, 2020; DOI: 10.3892/ijo.2019.4907]. |
| Databáze: | OpenAIRE |
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