Specific expression of the human voltage-gated proton channel Hv1 in highly metastatic breast cancer cells, promotes tumor progression and metastasis

The newly discovered human voltage-gated proton channel Hv1 is essential for proton transfer, which contains a voltage sensor domain (VSD) without a pore domain. We report here for the first time that Hv1 is specifically expressed in the highly metastatic human breast tumor tissues, but not in poorly metastatic breast cancer tissues, detected by immunohistochemistry. Meanwhile, real-time RT-PCR and immunocytochemistry showed that the expression levels of Hv1 have significant differences among breast cancer cell lines, MCF-7, MDA-MB-231, MDA-MB-468, MDA-MB-453, T-47D and SK-BR-3, in which Hv1 is expressed at a high level in highly metastatic human breast cancer cell line MDA-MB-231, but at a very low level in poorly metastatic human breast cancer cell line MCF-7. Inhibition of Hv1 expression in the highly metastatic MDA-MB-231 cells by small interfering RNA (siRNA) significantly decreases the invasion and migration of the cells. The intracellular pH of MDA-MB-231 cells down-regulated Hv1 expression by siRNA is obviously decreased compared with MDA-MB-231 with the scrambled siRNA. The expression of matrix metalloproteinase-2 and gelatinase activity in MDA-MB-231 cells suppressed Hv1 by siRNA were reduced. Our results strongly suggest that Hv1 regulates breast cancer intracellular pH and exacerbates the migratory ability of metastatic cells.     

Human amelogenin up-regulates osteogenic gene expression in human bone marrow stroma cells

Extracts of enamel matrix proteins are used to regenerate periodontal tissues. Amelogenin, the most abundant enamel protein, plays an important role in the regeneration of these tissues. However, the molecular mechanisms by which amelogenin contributes to periodontal regeneration remain unknown. Using primary human bone marrow stroma cells (hBMSCs) transduced with lentivirus encoding human amelogenin (hAm), we performed genome-wide expression profiling to analyze the effects of hAm transduction on the regulation of genes involved in osteogenic differentiation. Our results revealed that BMP-2, BMP-6, OPN and VEGFC were up-regulated. These results suggest that hAm may be a key element in regulating hBMSCs osteogenic differentiation.     

Synthesis, crystal structure and magnetic properties of cubane and linear trinuclear nickel complexes formed by 3,5-dichloro-2-hydroxybenzylaminoacetic acid

The reaction of Ni(ClO₄)₂·6H₂O with 3,5-dichloro-2-hydroxy-benzylaminoacetic acid (H₂dchaa), NaN₃ and triethylamine in methanol solution or water solution under solvothermal methods leads to the formation of two completely different Ni^II compounds: [HN(C₂H₅)₃]₈·[Ni₄(dchaa)₄(N₃)₄]₂ (1) and [HN(C₂H₅)₃]₂·[Ni₃(dchaa)₄(H₂O)₄]₂·(H₂O)₂ (2). The complexes 1 and 2 have been characterized by elemental analyses, IR spectra and single-crystal X-ray diffraction. Structure analyses reveal that complex 1 is a cubane cluster, while the complex 2 is a linear trinuclear cluster. The magnetic investigation shows that complexes 1 and 2 exhibit a ferromagnetic coupling between Ni^II ions. Ac susceptibilities of 1 and 2 reveal no frequency-dependent out-of-phase signals and the corresponding magnetic properties were discussed.     

Genome sequence of Agrobacterium tumefaciens strain F2, a bioflocculant-producing bacterium

Agrobacterium tumefaciens F2 is an efficient bioflocculant-producing bacterium. But the genes related to the metabolic pathway of bioflocculant biosynthesis in strain F2 are unknown. We present the draft genome of A. tumefaciens F2. It could provide further insight into the biosynthetic mechanism of polysaccharide-like bioflocculant in strain F2.     

Complete genome sequence of seawater bacterium Glaciecola nitratireducens FR1064(T)

Glaciecola nitratireducens strain FR1064(T) was isolated from seawater and described as a new species by Baik et al. in 2006. The genome size is about 1.01 to 1.26 Mb smaller than two reported Glaciecola genomes, indicating the gain or loss of large genome segments in the evolution of Glaciecola strains.     

Mutant p53 disrupts role of ShcA protein in balancing Smad protein-dependent and -independent signaling activity of transforming growth factor-β (TGF-β)

Biomarkers are lacking for identifying the switch of transforming growth factor-β (TGF-β) from tumor-suppressing to tumor-promoting. Mutated p53 (mp53) has been suggested to switch TGF-β to a tumor promoter. However, we found that mp53 does not always promote the oncogenic role of TGF-β. Here, we show that endogenous mp53 knockdown enhanced cell migration and phosphorylation of ERK in DU145 prostate cancer cells. Furthermore, ectopic expression of mp53 in p53-null PC-3 prostate cancer cells enhanced Smad-dependent signaling but inhibited TGF-β-induced cell migration by down-regulating activated ERK. Reactivation of ERK by the expression of its activator, MEK-1, restored TGF-β-induced cell migration. Because TGF-β is known to activate the MAPK/ERK pathway through direct phosphorylation of the adaptor protein ShcA and MAPK/ERK signaling is pivotal to tumor progression, we investigated whether ShcA contributed to mp53-induced ERK inhibition and the conversion of the role of TGF-β during carcinogenesis. We found that mp53 expression led to a decrease of phosphorylated p52ShcA/ERK levels and an increase of phosphorylated Smad levels in a panel of mp53-expressing cancer cell lines and in mammary glands and tumors from mp53 knock-in mice. By manipulating ShcA levels to regulate ERK and Smad signaling in human untransformed and cancer cell lines, we showed that the role of TGF-β in regulating anchorage-dependent and -independent growth and migration can be shifted between growth suppression and migration promotion. Thus, our results for the first time suggest that mp53 disrupts the role of ShcA in balancing the Smad-dependent and -independent signaling activity of TGF-β and that ShcA/ERK signaling is a major pathway regulating the tumor-promoting activity of TGF-β.     

The roles of ascorbic acid and glutathione in symptom alleviation to SA-deficient plants infected with RNA viruses

Salicylic acid (SA) is required for plant systemic acquired resistance (SAR) to viruses. However, SA-deficient plants adapt to RNA virus infections better, which show a lighter symptom and have less reactive oxygen species (ROS) accumulation. The virus replication levels are higher in the SA-deficient plants during the first 10?days, but lower than the wild-type seedlings after 20?dpi. The higher level of glutathione and ascorbic acid (AsA) in SA-deficient plants may contribute to their alleviated symptoms. Solo virus-control method for mortal viruses results in necrosis and chlorosis, no matter what level of virus RNAs would accumulate. Contrastingly, early and high-dose AsA treatment alleviates the symptom, and eventually inhibits virus replication after 20?days. ROS eliminators could not imitate the effect of AsA, and could neither alleviate symptom nor inhibit virus replication. It suggests that both symptom alleviation and virus replication control should be considered for plant virus cures.     

Aletris simpliciflora sp. nov. (Nartheciaceae) from southwest Xizang,China

Aletris simpliciflora R. Li & S. D. Zhang, a new species of Nartheciaceae from southwest Xizang, China, is described and illustrated. It is similar, and apparently closely related, to A. nana S. C. Chen, but differs by having usually solitary flower, pubescent bract and bracteole, and distinct filaments ca 1.2 mm long.