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Protein profiling and identification of modulators regulated by the E7 oncogene in the C33A cell line by proteomics
Kyung-Ae Lee1, Jung-Hyun Shim, Chang Won Kho
1Laboratory of Cellular Biology, Korea Research Institute of Bioscience and Biotechnology, Yuseong, Daejeon, Korea.
Abstract:
Human papillomaviruses (HPVs) have been recognized as the primary cause of cervical cancer. HPV 16 E7 binds to tumor suppressor retinoblastoma protein, and interferes with its function, causing release of the transcription factor E2F, which influences expression of cell cycle-related genes. This study was performed to identify the genes and proteins modulated by the HPV E7 oncogene. An HPV-negative cervical cancer cell line (C33A) was prepared to establish a stable cell line expressing E7. In order to analyze the target molecules modulated by E7 expression, we used two approaches: matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) and DNA microarrays. Forty-seven spots were identified in C33A/E7 by two-dimensional electrophoresis and MALDI/TOF MS. Protein disulfide isomerase A3, integrase interactor 1 protein, growth inhibitory protein, glutathione S-transferase P, and vav proto-oncogene were down-regulated, whereas heat shock 60 kDa protein 1, Ku70 binding protein, alpha enolase, 26S proteasome subunit were up-regulated. A genomic approach using a microarray kit showed that IL-12R beta 1, cytochrome c, and tumor necrosis factor receptor II were induced by the E7 oncogene. These results suggest that E7 can evade immune surveillance by suppressing or inducing these cell signaling factors, cell cycle regulators, and chaperones.
Insights
Human papillomavirus (HPV) E7 oncogene disrupts cell cycle regulation and immune evasion in cervical cancer. This study identified specific protein and gene expression changes induced by HPV E7.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Human papillomaviruses (HPVs) are the primary cause of cervical cancer.
- The HPV 16 E7 oncogene interferes with tumor suppressor proteins like retinoblastoma protein, affecting cell cycle control.
Purpose of the Study:
- To identify genes and proteins modulated by the HPV E7 oncogene in cervical cancer cells.
- To understand the molecular mechanisms of HPV-induced cervical carcinogenesis.
Main Methods:
- Utilized a stable HPV-negative cervical cancer cell line (C33A) engineered to express HPV E7.
- Employed matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) and DNA microarrays to analyze protein and gene expression changes.
Main Results:
- Identified 47 protein expression changes, including down-regulation of Protein disulfide isomerase A3 and up-regulation of alpha enolase.
- Genomic analysis revealed induction of IL-12R beta 1, cytochrome c, and tumor necrosis factor receptor II by the E7 oncogene.
- Observed modulation of cell signaling factors, cell cycle regulators, and chaperones.
Conclusions:
- HPV E7 oncogene significantly alters cellular protein and gene expression profiles.
- These alterations likely contribute to cervical cancer development by affecting cell cycle regulation and promoting immune evasion.
