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A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
Published on: April 12, 2017
CENPF promotes the proliferation of renal cell carcinoma in vitro
Ji Zhang1, Zhenyu Wang1, Zhenmin Liu1
1Department of Urology, Nantong First People's Hospital, Second Affiliated Hospital of Nantong University, Nantong, China.
Background:
Metastasis and drug resistance are the main causes of renal cell carcinoma (RCC) mortality. Currently, there are still a limited number of targeted therapies against advanced RCC. It is critical to develop new effective clinical biomarkers and drug targets in RCC. Several studies have shown that centromere protein F (CENPF), a microtubule binding protein, promotes cancer progression in various types of cancer. The purpose of this study was to explore the role of CENPF in RCC.
Methods:
Peripheral blood and corresponding tissue samples of 23 RCC patients and 23 normal physical examination patients who were treated in our hospital from 2018 to 2020 were collected, and CENPF expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemical (IHC) methods. The expression of CENPF was downregulated by small interfering RNA (siRNA) transfection, and the proliferation of the corresponding RCC cells and the corresponding cell cycle were detected.
Results:
According to The Cancer Genome Atlas (TCGA) data analysis, CENPF is highly expressed in RCC, and its expression level is significantly related to the overall survival (OS) and recurrence-free survival (RFS) of RCC. In addition, high expression of CENPF was found in the tissues of RCC patients in our hospital. Knockdown of CENPF significantly reduced the proliferation of RCC cells in vitro, and knockdown of CENPF regulated the cell cycle by inhibiting the expression of cyclins such as CDK4, CDK6, and CyclinD1.
Conclusions:
CENPF can be used as an independent prognostic factor of RCC and regulate the proliferation ability and cell cycle of RCC cells. CENPF is a potential oncogene and prognostic marker in RCC.
Insights
Centromere protein F (CENPF) is highly expressed in renal cell carcinoma (RCC) and promotes cancer progression. Downregulating CENPF inhibits RCC cell proliferation and regulates the cell cycle, identifying CENPF as a potential prognostic marker.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Metastasis and drug resistance are primary drivers of renal cell carcinoma (RCC) mortality.
- Limited targeted therapies exist for advanced RCC, necessitating novel biomarkers and drug targets.
- Centromere protein F (CENPF), a microtubule-associated protein, is implicated in promoting cancer progression across various malignancies.
Purpose of the Study:
- To investigate the role and clinical significance of CENPF in renal cell carcinoma (RCC).
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) data.
- Quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemistry (IHC) on RCC patient samples.
- In vitro studies involving CENPF knockdown using small interfering RNA (siRNA) to assess effects on RCC cell proliferation and cell cycle progression.
Main Results:
- CENPF is highly expressed in RCC, with expression levels correlating significantly with overall survival (OS) and recurrence-free survival (RFS).
- High CENPF expression was confirmed in RCC patient tissues.
- Knockdown of CENPF suppressed RCC cell proliferation and altered cell cycle regulation by inhibiting key cyclins (e.g., CDK4, CDK6, CyclinD1).
Conclusions:
- CENPF serves as an independent prognostic factor in RCC.
- CENPF regulates RCC cell proliferation and cell cycle.
- CENPF is identified as a potential oncogene and prognostic marker for RCC.
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