CDK7 activated beta‐catenin/TCF signaling in hepatocellular carcinoma

&NA; 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.

• Publication year

  2018

• Venue

  Experimental Cell Research

• Publication date

  2018-09-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.yexcr.2018.07.010PMID 29981747
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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