AI Article Synopsis

  • CCDC25 is found to be overexpressed in clear cell renal cell carcinoma (ccRCC) tissues and cell lines compared to normal tissues, indicating its potential role in cancer development.
  • Experiments showed that knocking down CCDC25 significantly inhibited tumor growth, migration, and invasion of cancer cells, while overexpressing it had the opposite effect.
  • The study suggests that CCDC25 interacts with integrin-linked kinase (ILK) to activate the NF-κB signaling pathway, making it a promising target for therapeutic interventions in ccRCC.

Article Abstract

Increasing evidence has demonstrated that the expression of coil domains containing 25 (CCDC25) in various malignancies is abnormally high. However, the potential regulatory role and mechanism of CCDC25 in the development of clear cell renal cell carcinoma (ccRCC) are still unclear. In this experiment, we combined in vitro experiments such as wound healing, CCK8, and transwell assay with in vivo experiments on tumor formation in nude mice to evaluate the effect of CCDC25 on the proliferation, migration, and invasion of renal cancer cells. In addition, we also used Western blotting and qPCR to evaluate the role of CCDC25 in activating the integrin-linked kinase (ILK)-NF-κB signaling pathway. Here, we demonstrate that compared to normal tissues and cell lines, CCDC25 is overexpressed in both human ccRCC tissues and cell lines. After CCDC25 knockdown, it has obvious inhibitory effect on the proliferation, migration, and invasion of cancer cells in vitro and in vivo. In contrast, CCDC25 overexpression promotes these effects. Additionally, we also discovered that CCDC25 interacts with ILK and coordinates the activation of the NF-κB signaling pathway downstream. Generally, our study suggests that CCDC25 plays a vital role in the development of ccRCC, which also means that it may be a potential therapeutic target for ccRCC.

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Source
http://dx.doi.org/10.1096/fj.202301064RRDOI Listing

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