CENPF promotes the proliferation of renal cell carcinoma in vitro

Transl Androl Urol. 2023 Feb 28;12(2):320-329. doi: 10.21037/tau-22-797. Epub 2023 Feb 27.

Abstract

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.

Keywords: Renal cell carcinoma (RCC); cell cycle regulation; cell proliferation; centromere protein F (CENPF).