The role of gC1qR in regulating survival of human papillomavirus 16 oncogene-transfected cervical cancer cells
| Autor: | Xi-Rong Guo, Zhu Liu, Ling-juan Gao, Feng Qiu, Wei-Min Fan, Yu-Zhu Peng, Ping-Qing Gu |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Cancer Research
Cell Survival Cell Uterine Cervical Neoplasms Apoptosis Mitochondrion Biology Transfection medicine.disease_cause Mitochondrial Proteins Immune system Cell Line Tumor medicine Humans Human papillomavirus 16 Oncogene Electron Transport Complex II Oncogene Proteins Viral Mitochondria Protein Transport medicine.anatomical_structure Oncology Cancer cell Immunology Cancer research Calcium Female Carrier Proteins Reactive Oxygen Species Carcinogenesis |
| Zdroj: | International Journal of Oncology. |
| ISSN: | 1791-2423 1019-6439 |
| DOI: | 10.3892/ijo.2011.1108 |
| Popis: | Human papillomavirus 16 (HPV-16) is strongly associated with the development of 50% of cervical cancers. The E6 and E7 proteins encoded by high-risk HPV types are associated with the immune evasion of cervical cancer cells, but the mechanism is poorly understood. The purpose of this study was to investigate whether cells transfected with E6 and E7 expression constructs reduce the expression of the globular heads of the C1q receptor (gC1qR), a mitochondrial surface protein overexpressed in certain cancer cells. First, C-33A cells were transiently transfected with the HPV-16 E6 and E7 oncogenes which resulted in gC1qR inhibition and a reduction in apoptosis. Second, gC1qR overexpression in cells showed that caspase-3 activation and mitochondrial dysfunction were involved in gC1qR-induced apoptosis. Cells transfected with a GFP-gC1qR vector resulted in upregulated gC1qR protein and a gradual increase in the generation of reactive oxygen species (ROS). Additionally, ROS generation and increased Ca2+ influx in mitochondria resulted in the loss of the mitochondrial transmembrane potential. Interestingly, when gC1qR was overexpressed in C-33A cells, apoptosis was significantly inhibited when cells were treated with metformin, which may protect mitochondrial function. These data suggest that gC1qR could play an important role in HPV-16-induced cervical cancer immune evasion depending on its level of expression and subcellular localisation. |
| Databáze: | OpenAIRE |
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