It is increasingly clear that hepatocellular carcinoma (HCC) has a distinct microRNA (miRNA) expression profile that is involved in malignancy; however, little is known about how functional miRNA modulates the metastasis of hepatitis B virus (HBV)-related HCC (HBV-HCC). In the present study, we demonstrate that the levels of miRNA-143 (miR-143) are dramatically increased in metastatic HBV-HCC of both p21-HBx transgenic mice and HCC patients. Moreover, we show that overexpression of this miRNA is transcribed by nuclear factor kappa B (NF-B) and favors liver tumor cell invasive and metastatic behavior. H epatocellular carcinoma (HCC) is a common and aggressive cancer that is strongly associated with chronic infection by the hepatitis B virus (HBV). 1 Poor prognosis and patient survival with HCC are largely due to invasion/metastasis and postsurgical recurrence. 2 The HBV X protein (HBx), a protein encoded by HBV, is thought to play a key role in the molecular pathogenesis of HBV-related HCC (HBV-HCC). 2,3 Invasion and metastasis are fundamental properties of HBV-HCC, which has a very high mortality rate. Alteration of some adhesion molecules in HBV-HCC has been described, including up-regulation of matrix metalloproteinases 1-3 and down-regulation of E-cadherin. Both of these changes indicate that HBx contributes to the metastatic spread of liver tumors. 2,4 Metastasis is a complex cascade, however, and the underlying molecular mechanisms are far from being fully understood.MicroRNAs (miRNAs) are evolutionarily endogenous regulatory noncoding RNAs that play critical roles in gene regulation. 5 Recent studies implicate miRNAs in several cancers, and altered miRNA levels can result in aberrant expression of gene products that may contribute to cancer biology, including tumor metastasis. [5][6][7][8] These findings suggest that expression profiling of miRNAs is an alternative method for cancer subtype classification, prognostication, and treatment. 5,7,8 It is known that HCC develops several years after HBV infection. 2,9 A p21-HBx transgenic mouse model was established by introducing the HBx gene into the p21 locus. About 60% of p21-HBx transgenic mice develop hepato-

Two-dimensional boron materials have recently attracted extensive theoretical interest because of their exceptional structural complexity and remarkable physical and chemical properties. However, such 2D boron monolayers have still not been synthesized. In this report, the synthesis of atomically thin 2D γ-boron films on copper foils is achieved by chemical vapor deposition using a mixture of pure boron and boron oxide powders as the boron source and hydrogen gas as the carrier gas. Strikingly, the optical band gap of the boron film was measured to be around 2.25 eV, which is close to the value (2.07 eV) determined by first-principles calculations, suggesting that the γ-B28 monolayer is a fascinating direct band gap semiconductor. Furthermore, a strong photoluminescence emission band was observed at approximately 626 nm, which is again due to the direct band gap. This study could pave the way for applications of two-dimensional boron materials in electronic and photonic devices.

Octamer 4 (Oct4), a member of the POU family of transcription factors, plays a key role in the maintenance of pluripotency and proliferation potential of embryonic stem cells. Cancer stem cell-like cells (CSCLC) are reported to be a minor population in tumors or even in tumor cell lines which also express Oct4. The role of Oct4 in CSCLCs still remains to be defined. In our study, we show that, in vitro, almost all murine Lewis lung carcinoma 3LL cells and human breast cancer MCF7 cells express Oct4 at high levels. This expression of Oct4 is successfully reduced by small interfering RNA, which eventually results in cell apoptosis. The signal pathway Oct4/ Tcl1/Akt1 has been observed to be involved in this event. The repression of Oct4 reduces Tcl1 expression and further downregulates the level of p-Ser.473-Akt1. In vivo, only f5% of tumor cells were detected to express Oct4 in established 3LL and MCF7 tumor models, respectively. Small interfering RNA against Oct4 successfully decreases the CSCLCs and markedly inhibits tumor growth. In summary, we show that Oct4 might maintain the survival of CSCLCs partly through Oct4/Tcl1/ Akt1 by inhibiting apoptosis, which strongly indicates that targeting Oct4 may have important clinical applications in cancer therapy. [Cancer Res 2008;68(16):6533-40]

Ultrathin crystalline Mo3B films have been synthesized on molybdenum foils, exhibiting striking catalytic performance and fantastic cycling stability.