Shu-Hao Hsu

TL;DR: It is demonstrated that deletion of mouse Mir122 resulted in hepatosteatosis, hepatitis, and the development of tumors resembling HCC, demonstrating critical functions for miR-122 in the maintenance of liver homeostasis and have important therapeutic implications, including the potential utility of mi R-122 delivery for selected patients with HCC and the need for careful monitoring of patients receiving miR -122 inhibition therapy for HCV.

TL;DR: It is suggested that the loss of multifunctional miR-122 contributes to the malignant phenotype of HCC cells, and mi R-122 mimetic alone or in combination with anticancer drugs can be a promising therapeutic regimen against liver cancer.

TL;DR: The global steady-state measurements are extended to additional mammalian contexts and find that regardless of the miRNA, cell type, growth condition, or translational state, mRNA destabilization explains most (66%->90%) miRNA-mediated repression.

TL;DR: Upregulation of miR-181b at early stages of feeding CDAA diet promotes hepatocarcinogenesis and enhanced resistance of HCC cells to the anticancer drug doxorubicin.

TL;DR: It is concluded that gluconeogenesis is severely compromised in HCC by IL6‐Stat3‐mediated activation of miR‐23a, which directly targets PGC‐1α and G6PC, leading to decreased glucose production.