CDK7 activated beta-catenin/TCF signaling in hepatocellular carcinoma.

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.

Duan J ，He Y ，Fu X ，Deng Y ，Zheng M ，Lu D ... -  《-》

PKMYT1 promoted the growth and motility of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling.

Over-activation of beta-catenin/TCF signaling has been frequently observed in hepatocellular carcinoma (HCC). Better understanding the molecular mechanism for the aberrant activation of beta-catenin/TCF signaling would provide novel insights into the treatment of this malignancy. In this study, we have shown that the expression of PKMYT1 was up-regulated in HCC. PKMYT1 positively regulated the growth, migration, colony formation, metastasis and epithelia mesenchymal transition (EMT) of HCC cells. Mechanically, PKMTY1 activated the beta-catenin/TCF signaling by binding and inactivating GSK3beta. Taken together, our study demonstrated the oncogenic activity of PKMYT1 in the progression of HCC and suggested that PKMYT1 might be a therapeutic target.

Liu L ，Wu J ，Wang S ，Luo X ，Du Y ，Huang D ，Gu D ，Zhang F ... -  《-》

CARF activates beta-catenin/TCF signaling in the hepatocellular carcinoma.

Fan X ，Ma X ，Cui L ，Dang S ，Qu J ，Zhang J ，Wang X ，Mao Z ... -  《Oncotarget》

STIP1 is over-expressed in hepatocellular carcinoma and promotes the growth and migration of cancer cells.

Wnt/beta-catenin signaling is frequently activated in hepatocellular carcinoma (HCC). Better understanding the mechanism for its over-activation would help the therapy. In this study, we have shown that the stress-induced phosphoprotein 1 (STIP1) is up-regulated in the HCC tissues. Functional studies showed that STIP1 promoted the growth, colony formation and migration of cancer cells. However, knocking down the expression of STIP1 inhibited the growth, colony formation and migration of cancer cells. Molecular mechanism study showed that STIP1 interacted with Axin, enhanced the interaction between Axin and DVL2, thus activated beta-catenin/TCF signaling. Taken together, our study demonstrated the oncogenic roles of STIP1 in the progression of HCC, and suggested that STIP1 might be a therapeutic target.

Luo X ，Liu Y ，Ma S ，Liu L ，Xie R ，Li M ，Shen P ，Wang S ... -  《-》

DIAPH3 promoted the growth, migration and metastasis of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling.

Dong L ，Li Z ，Xue L ，Li G ，Zhang C ，Cai Z ，Li H ，Guo R ... -  《-》