Death rate from HCC is increasing and liver cancer is the second leading cause of cancer-related mortality worldwide. Most patients with HCC have underlying liver cirrhosis and compromised liver function, limiting treatment options. Cirrhosis is associated with cell dedifferentiation and expansion of hepatocholangiolar progenitor cells. We identified a miRNA signature associated with HCC and hepatocytic differentiation of progenitor cells. We further identified miR-148a as an inducer of hepatocytic differentiation that is downregulated in HCC. MiR-148a-mimetic treatment in vivo suppressed tumor growth, reduced tumor malignancy and liver fibrosis, and prevented tumor development. These effects were associated with an increased differentiated phenotype and were mediated by IKKα/NUMB/NOTCH signaling. Conclusion our results identified miR-148a as an inhibitor of the IKKα/NUMB/NOTCH pathway and an inducer of hepatocytic differentiation that when deregulated promotes HCC initiation and progression. This study represents the first evidence that differentiation-targeted therapy is a promising strategy to treat and prevent HCC.

Bismuth oxyhalides with layered structures have emerged as an important class of photocatalysts but usually suffer from low activity largely due to their unfavorable band structures. Although point defects as typical electronic structure modifiers have been actively used to modify electronic structures of photocatalysts for high photocatalytic activity, the underlying role of halogen vacancies in improving activity of bismuth oxyhalides has been overlooked. In this study, we demonstrate the substantial role of iodine vacancies in enabling photocatalytic activity of BiOI as a model oxyhalide photocatalyst. It is found that iodine vacancies cause a 0.23 eV downward shift of the valence band maximum of BiOI but not much change in the bandgap. Such band structure modification leads to the formation of photogenerated holes with a stronger oxidative ability, which is favorable for photocatalysis with the holes induced half reaction as a rate-determining step. The results obtained might provide an important implication in designing highly efficient oxyhalide-based photocatalysts by controlling halogen vacancies.

Purpose: Liver cancer, one of the most common cancers in China, is reported to feature relatively high morbidity and mortality. Curcumin (Cum) is considered as a drug possessing anti-angiogenic, anti-inflammation and anti-oxidation effect. Previous research has demonstrated antitumor effects in a series of cancers. Materials and Methods: In this study the in vitro cytotoxicity of Cum was measured by MTT assay and pro-apoptotic effects were assessed by DAPI staining and measurement of caspase-3 activity. In vivo anti-hepatoma efficacy of Cum was assessed with HepG2 xenografts. Results: It is found that Cum dose-dependently inhibited cell growth in HepG2 cells with activation of apoptosis. Moreover, Cum delayed the growth of liver cancer in a dose-dependent manner in nude mice. Conclusions: Cum might be a promising phytomedicine in cancer therapy and further efforts are needed to explore this therapeutic strategy.

Granulocyte-colony-stimulating factor (G-cSF) is a member of the hematopoietic growth factor family that primarily affects the neutrophil lineage. G-cSF serves as a powerful mobilizer of peripheral blood stem cells and recombinant human G-cSF (rhG-cSF) has been used to treat granulocytopenia and neutropenia after chemotherapy for cancer patients. However, recent studies have found that G-cSF plays an important role in cancer progression. G-cSF expression is increased in different types of cancer cells, such as lung cancer, gastric cancer, colorectal cancer, invasive bladder carcinoma, glioma and breast cancer. However, it is unclear whether treatment with G-cSF has an adverse effect. The current review provides an overview of G-cSF in malignant breast cancer development and the data presented in this review are expected to provide new ideas for cancer therapy. Contents 1. introduction 2. Structure of the G-cSF gene 3. regulation of G-cSF gene expression 4. The G-cSF receptor 5. G-cSF expression in breast cancer 6. direct effects of G-cSF on breast cancer 7. role of tumor microenvironment in the effect of G-cSF on breast cancer 8. conclusions

MicroRNA expression profiling in human liver progenitor cells following hepatocytic differentiation identified miR-122 and miR-194 as the microRNAs most strongly upregulated during hepatocytic differentiation of progenitor cells. MiR-194 was also highly upregulated following hepatocytic differentiation of human embryonic stem cells (hESCs). Overexpression of miR-194 in progenitor cells accelerated their differentiation into hepatocytes, as measured by morphological features such as canaliculi and expression of hepatocytic markers. Overexpression of miR-194 in hESCs induced their spontaneous differentiation, a phenotype accompanied with accelerated loss of the pluripotent factors OCT4 and NANOG and decrease in mesoderm marker HAND1 expression. We then identified YAP1 as a direct target of miR-194. Inhibition of YAP1 strongly induced hepatocytic differentiation of progenitor cells and YAP1 over expression reversed the miR-194-induced hepatocytic differentiation of progenitor cells. In conclusion, we identified miR-194 as a potent inducer of hepatocytic differentiation of progenitor cells and further identified YAP1 as a mediator of miR-194's effects on hepatocytic differentiation and liver progenitor cell fate.