CSNK2B contributes to colorectal cancer cell proliferation by activating the mTOR signaling
Shijun Yu1, Qingqing Hu1, Kailing Fan1
1Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, 150 Ji-Mo Road, Shanghai, 200120, People's Republic of China.
Abstract:
The function of Casein kinase 2 beta (CSNK2B) in human malignancies has drawn increasing attention in recent years. However, its role in colorectal cancer (CRC) remains unclear. In the present study, we aimed to explore the expression and biological functions of CSNK2B in CRC. Public gene expression microarray data from online database and immunohistochemistry analysis demonstrated that CSNK2B was highly expressed in CRC tissues than in normal tissues. In vitro and in vivo cellular functional experiments showed that increased CSNK2B expression promoted CRC cell viability and tumorigenesis of CRC. Further western blots and rescue experiments confirmed that CSNK2B promoted CRC cell proliferation mainly by activating the mTOR signaling pathway. These findings identified CSNK2B as a novel oncogene contributing to the development of CRC.
Insights
Casein kinase 2 beta (CSNK2B) is highly expressed in colorectal cancer (CRC) and promotes tumor growth by activating the mTOR pathway, identifying it as a potential oncogene.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The role of Casein kinase 2 beta (CSNK2B) in human cancers is gaining attention.
- Its specific function in colorectal cancer (CRC) pathogenesis is not well understood.
Purpose of the Study:
- To investigate the expression and biological functions of CSNK2B in colorectal cancer.
- To elucidate the molecular mechanisms underlying CSNK2B's role in CRC development.
Main Methods:
- Analysis of public gene expression microarray data.
- Immunohistochemistry staining of CRC tissues.
- In vitro and in vivo cellular functional assays.
- Western blot analysis and rescue experiments.
Main Results:
- CSNK2B expression was significantly higher in CRC tissues compared to normal tissues.
- Elevated CSNK2B expression enhanced CRC cell viability and tumorigenesis.
- CSNK2B promotes CRC cell proliferation via activation of the mTOR signaling pathway.
Conclusions:
- CSNK2B acts as a novel oncogene in colorectal cancer.
- Targeting CSNK2B may offer a potential therapeutic strategy for CRC.
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