2022•Research SquareOpen access

CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma

Xun Wang, Jie Liu, Qiang Liu, Jiale Zhou, Wen Kong, Yiran Huang, Wei Xue, Fan Yang, Jiwei Huang

Open full text 1 citations

Abstract

Abstract Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer in adult, and patients with advanced ccRCC are facing limited treatment options. Cell division cycle associated 5 (CDCA5), a key regulator for segregating sister chromatids in cell cycle, has been increasingly reported for a potential therapeutic target in multiple human cancers. However, the functional roles of CDCA5 in ccRCC remain uncertain. Here we identified that CDCA5 expression was frequently upregulated in ccRCC tumors and significantly associated with poor prognosis of ccRCC patients. To investigate the role of CDCA5 in ccRCC progression, loss function cell models were established. Knockdown of CDCA5 remarkably suppressed ccRCC cell proliferation and migration ability, and also induced cell apoptosis in vitro. In addition, the significance of CDCA5 in ccRCC was further demonstrated in a mouse xenograft model. Silencing of CDCA5 drastically inhibited in vivo tumorigenicity of ccRCC cells. Mechanically, we identified CDCA5 may cooperate with EEF1A1 to promote the tumorigenic phenotype of ccRCC. Overall, our results revealed the significant functional role of CDCA5 in ccRCC progression, which may pave a way for the development of new treatment strategies for ccRCC treatment.

Open-access reader

About this research paper

What this paper is about

Abstract Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer in adult, and patients with advanced ccRCC are facing limited treatment options. Cell division cycle associated 5 (CDCA5), a key regulator for segregating sister chromatids in cell cycle, has been increasingly reported for a potential therapeutic target in multiple human cancers. However, the functional roles of CDCA5 in ccRCC remain uncertain. Here we identified that CDCA5 expression was frequently upregulated in ccRCC tumors and significantly associated with poor prognosis of ccRCC patients. To investigate the role of CDCA5 in ccRCC progression, loss function cell models were established. Knockdown of CDCA5 remarkably suppressed ccRCC cell proliferation and migration ability, and also induced cell apoptosis in vitro. In addition, the significance of CDCA5 in ccRCC was further demonstrated in a mouse xenograft model. Silencing of CDCA5 drastically inhibited in vivo tumorigenicity of ccRCC cells. Mechanically, we identified CDCA5 may cooperate with EEF1A1 to promote the tumorigenic phenotype of ccRCC. Overall, our results revealed the significant functional role of CDCA5 in ccRCC progression, which may pave a way for the development of new treatment strategies for ccRCC treatment.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Abstract Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer in adult, and patients with advanced ccRCC are facing limited treatment options. Cell division cycle associated 5 (CDCA5), a key regulator for segregating sister chromatids in cell cycle, has been increasingly reported for a potential therapeutic target in multiple human cancers. However, the functional roles of CDCA5 in ccRCC remain uncertain. Here we identified that CDCA5 expression was frequently upregulated in ccRCC tumors and significantly associated with poor prognosis of ccRCC patients. To investigate the role of CDCA5 in ccRCC progression, loss function cell models were established. Knockdown of CDCA5 remarkably suppressed ccRCC cell proliferation and migration ability, and also induced cell apoptosis in vitro. In addition, the significance of CDCA5 in ccRCC was further demonstrated in a mouse xenograft model. Silencing of CDCA5 drastically inhibited in vivo tumorigenicity of ccRCC cells. Mechanically, we identified CDCA5 may cooperate with EEF1A1 to promote the tumorigenic phenotype of ccRCC. Overall, our results revealed the significant functional role of CDCA5 in ccRCC progression, which may pave a way for the development of new treatment strategies for ccRCC treatment.

Key concepts: Clear cell renal cell carcinoma, Cancer research, Cell growth, Cell cycle, Gene knockdown, Gene silencing, Cell, Apoptosis

Related papers

Back to paper searchBrowse research topicsOriginal source
CDCA5 is a potent therapeutic target of clear cell renal cell carcinoma — Research Paper | ScholarLens