Bone morphogenetic protein is a key regulation factor in osteoplast cell differentiation and bone formation.It takes a role of differentiation inducting and orientating by modulating the transcription factor and through some unknown signal transduction pathway,and its expression and function can be adjusted by signal transducting system and specific acceptor inhibiter.This article reviews the research progresses on the aspects.

ObjectiveTo investigate the inhibitory effect of lentivirusly-mediated ObR-siRNA on transplanted MCF-7 human breast cancer cells by intratumoral injection.MethodsA model of subcutaneous implanted tumor was generated through injecting MCF-7 human breast cancer cells into the nude mice.Thirty established mice with MCF-7 breast cancer cells xenograft were divided into 3 groups randomly,and mice in the experimental group were intratumorally injected with ObR-siRNA lentivirus,while the negative control group and blank control group mice were injected with the same dose of negative lentivirus and normal saline.All mice were subcutaneously injected with recombinant human leptin around the tumor site once a day.Tumor size was blindly measured every other day and the mRNA expression and protein expression levels of ObR in each group were determined.ResultsKnockdown of ObR-treated xenografted nude mice with a high leptin microenvironment was successfully established.Local injection of ObR-siRNA lentivirus significantly suppressed the established tumor growth in nude mice(P ＜ 0.01,P ＜0.01 ).Real time-PCR and Western blotting showed that the mRNA and protein expression of ObR was decreased in the ObR-siRNA lentivirus group( P ＜ 0.01,P ＜ 0.01 ).ConclusionsIntratumoral injection of recomhinant ObR-siRNA lentivirus inhibits the growth of MCF-7 cells xenografts in the nude mice,suggesting that ObR might represent a therapeutic target in the genotherapies of human breast cancer.

To analyze the molecular basis of the variation of the pathogenicity of the influenza B virus, we rescued a recombinant virus with a deletion in the carboxyl terminal of the NS1 protein using reverse genetics based on the parental virus B-S9 of B/Yamagata/16/88. A mutant strain with a deletion of 171 amino acids in the carboxyl terminal of the NS1 protein was named "B-L5". BALB/c mice were inoculated with 3 X 105 EID50 of B-L5 and the parental virus B-S9, respectively. Then, weight changes, survival, and viral titers were documented. During 3 days post-inoculation (dpi) to 7 dpi, the weight of mice infected with B-S9 decreased. However, the weight of mice infected with B-L5 showed weight decreases only at 2 dpi, and quickly recovered at 3 dpi. B-S9 and B-L5 could replicate in the lungs of BALB/c mice. However, viral titers in the lungs of mice infected with B-L5 were 7900-times lower than those of mice infected with B-S9 at 3 dpi. Viral titers in the lungs of mice infected with B-L5 were not detected at 6 dpi. These results showed that, compared with the parent virus B-S9, the mutant virus B-L5 showed lower pathogenicity in BALB/c mice. Our study suggests that deletion of the carboxyl terminal of the NS1 protein decreases the pathogenicity of the influenza B virus. Establishment of a reverse-genetics system for the B influenza virus will provide a platform for studying its pathogenesis, and mechanism of transmission, and for developing live-attenuated influenza B virus vaccines.
Animals ; Body Weight ; Dogs ; Female ; HEK293 Cells ; Humans ; Influenza B virus ; genetics ; pathogenicity ; physiology ; Madin Darby Canine Kidney Cells ; Mice ; Mice, Inbred BALB C ; Sequence Deletion ; Survival Analysis ; Viral Load ; genetics ; Viral Nonstructural Proteins ; chemistry ; genetics ; Virulence