Down-Regulation of C3aR/C5aR Inhibits Cell Proliferation and EMT in Hepatocellular Carcinoma
| Autor: | Wenyan Zhou, Yawen Zhang, Chaofeng Tang, Genwang Wang, Sah Chandra Bhushan, Peng Yuan, Junzhi Leng, Bendong Chen, Jinlong Ma |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Cancer Research
Carcinoma Hepatocellular Epithelial-Mesenchymal Transition Vimentin Apoptosis lcsh:RC254-282 Flow cytometry 03 medical and health sciences 0302 clinical medicine Cell Line Tumor medicine Humans Epithelial–mesenchymal transition Receptor Anaphylatoxin C5a Cells Cultured 030304 developmental biology 0303 health sciences Gene knockdown biology medicine.diagnostic_test Cell growth Chemistry Liver Neoplasms hepatocellular carcinoma Cell Cycle Checkpoints Cell cycle lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Immunohistochemistry digestive system diseases Complement system Receptors Complement Gene Expression Regulation Neoplastic Oncology 030220 oncology & carcinogenesis biology.protein Cancer research Original Article C3aR/C5aR |
| Zdroj: | Technology in Cancer Research & Treatment Technology in Cancer Research & Treatment, Vol 19 (2020) |
| ISSN: | 1533-0338 1533-0346 |
| Popis: | Complement 3a (C3a) and complement 5a (C5a), small cleavage fragments generated by complement activation, has been previously shown to be obviously up-regulated in highly metastatic hepatocellular carcinoma (HCC) cells. However, their functional roles in HCC cells remains unclear. Here, we investigated the biological function of G protein-coupled receptor C3aR/C5aR using small interference RNA in HCC cells. Our data showed that C3aR and C5aR knockdown significantly inhibited the proliferation, migration and invasion of HCC cells using CCK-8, colony formation and transwell assays. Flow cytometry assay showed C3aR and C5aR knockdown induced cell cycle G0/G1 phase arrest and apoptosis in HCC cells. Moreover, we found down-regulation of C3aR/C5aR obviously down-regulated the expression of PCNA, Ki-67 and suppressed the epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin and vimentin) in HCC cells. Collectively, our data demonstrated that targeting C3aR/C5aR may hold promise for the treatment of HCC. |
| Databáze: | OpenAIRE |
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