CDK7 activated beta-catenin/TCF signaling in hepatocellular carcinoma

Journal Article · Sat Sep 15 04:00:00 EDT 2018 · Experimental Cell Research

DOI:https://doi.org/10.1016/J.YEXCR.2018.07.010· OSTI ID:23082630

Duan, Juan; He, Yan ^[1]; Fu, Xiaolin ^[2]; Deng, Yujie ^[3]; Zheng, Min ^[1]; Lu, Dongdong ^[4]

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1. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350122 (China)
2. Institute of Biomedical Sciences, Fudan University, Shanghai 200032 (China)
3. Department of Chemotherapy, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005 (China)
4. School of Life Science and Technology, Tongji University, Shanghai 200092 (China)

Over-activation of beta-catenin/TCF signaling is very common in the progression of hepatocellular carcinoma (HCC). The molecular mechanisms leading to the aberrant activation of beta-catenin/TCF signaling are not fully understood. In this study, it was found that CDK7 was up-regulated in HCC tissues and its expression inversely correlated with the survival of HCC patients. Functional study showed that CDK7 promoted the growth and migration of HCC cells, and knocking down the expression of CDK7 inhibited the growth of HCC cells in both liquid culture and soft agar. Mechanistically, CDK7 interacted with beta-catenin, enhanced the interaction between beta-catenin and TCF4, and activated beta-catenin/TCF signaling. Taken together, this study demonstrated the oncogenic roles of CDK7 in HCC and suggested that CDK7 might be a promising therapeutic target.

• OSTI ID: 23082630
• Journal Information: Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 2 Vol. 370; ISSN 0014-4827; ISSN ECREAL
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANIMAL TISSUES
HEPATOMAS
PLANT GROWTH
SIGNALS