During carcinogenesis, NF-κB mediates processes associated with deregulation of the normal control of proliferation, angiogenesis, and metastasis. Thus, suppression of NF-κB has been linked with chemoprevention of cancer. Accumulating findings reveal that heat shock protein 90 (HSP90) is a molecular chaperone and a component of the IκB kinase (IKK) complex that plays a central role in NF-κB activation. HSP90 also stabilizes key proteins involved in cell cycle control and apoptosis signaling. We have determined whether the exogenous administration of isoflavone-deprived soy peptide prevents 7,12-dimethylbenz[α]anthracene (DMBA)-induced rat mammary tumorigenesis and investigated the mechanism of action. Dietary administration of soy peptide (3.3 g/rat/day) significantly reduced the incidence of ductal carcinomas (50%), the number of tumors per multiple tumor-bearing rats (49%; P < 0.05), and extended the latency period of tumor development (8.07 ± 0.92 weeks) compared to control diet animals (10.80 ± 1.30; P < 0.05). Our results have further demonstrated that soy peptide (1) dramatically inhibits the expression of HSP90, thereby suppressing signaling pathway leading to NF-κB activation; (2) induces expression of p21, p53, and caspase-3 proteins; and (3) inhibits expression of VEGF. In agreement with our in vivo data, soy peptide treatment inhibited the growth of human breast MCF-7 tumor cells in a dose-dependent manner and induced apoptosis. Taken together, our in vivo and in vitro results suggest chemopreventive and tumor suppressive functions of isoflavone-deprived soy peptide by inducing growth arrest and apoptosis.
Previously, we demonstrated that the homeoprotein Msx1 interaction with p53 inhibited tumor growth by inducing apoptosis. However, Msx1 can exert its tumor suppressive effect through the inhibition of angiogenesis since growth of the tumor relies on sufficient blood supply from the existing vessels to provide oxygen and nutrients for tumor growth. We hypothesized that the inhibition of tumor growth by Msx1 might be due to the inhibition of angiogenesis. Here, we explored the role of Msx1 in angiogenesis. Overexpression of Msx1 in HUVECs inhibited angiogenesis, and silencing of Msx1 by siRNA abrogated its anti-angiogenic effects. Furthermore, forced expression of Msx1 in mouse muscle tissue inhibited vessel sprouting, and application of an Ad-Msx1-transfected conditioned medium onto the chicken chorioallantoic membrane (CAM) led to a significant inhibition of new vessel formation. To explore the underlying mechanism of Msx1-mediated angiogenesis, yeast two-hybrid screening was performed, and we identified PIASy (protein inhibitor of activated STAT Y) as a novel Msx1-interacting protein. We mapped the homeodomain of Msx1 and the C-terminal domain of PIASy as respective interacting domains. Consistent with its anti-angiogenic function, overexpression of Msx1 suppressed the reporter activity of VEGF. Interestingly, PIASy stabilized Msx1 protein, whereas deletion of the Msx1-interacting domain in PIASy abrogated the inhibition of tube formation and the stabilization of Msx1 protein. Our findings suggest the functional importance of PIASy-Msx1 interaction in Msx1-mediated angiogenesis inhibition.
The changes in mechanical properties and thermal conductivities of fiber reinforced foam glass produced by adding 0~50 wt% basalt-fibers to 10 µm glass powder containing 6 wt% nanocarbon via low-temperature sintering at 750°C were examined. The prepared basalt-fibers had an aspect ratio of 70.88. To study the microstructure of the foam glass, optical microscopy and scanning electron microscopy were conducted. To assess the mechanical properties and thermal conductivity of the sample, a compressive strength tester and a heat flowmeter were used, respectively. The sample was confirmed to have closed pores up to the addition of 15 wt% basalt-fiber, with open pores being observed from 20 wt% or more. Microstructure analysis showed that the sample was shown to have dense basalt-fiber clusters with an even distribution of pores at 13 wt% basalt-fibers, whereas irregular pores formed with more basaltfiber addition. Compressive strength was increased by approximately 48 % compared to the sample without basalt-fiber addition while the sample with 13 wt% basalt-fibers showed gradual improvement up to a total of 2.96 MPa and then a gradual decrease with more addition. The thermal conductivity was seen to increase from 0.16 to 0.28 W/m•K with increasing basalt-fiber addition; nevertheless, the properties were suitable for using the samples as a thermal insulator.
As a blowing agent, 2-10 wt% of nanocarbon (NC) was added 10 µm glass powder (CaO, MgO, Al 2 O 3 , SO 3 , 83 wt%-SiO 2) and sintered at 700-900°C to fabricate foamed glasses with closed pores that were 62-2200 µm. Optical microscopy was used to examine the microstructure and pore size. Compressive strength tester and a heat flow meter were used to examine the changes in mechanical strength and thermal conductivity. The microstructure examination results showed that was performed at 700°C, 297.9-351.3 µm pores were fabricated, and the porosity was 57-63 % in the sample that contained 6-10 wt% NC. At sintering temperatures above 750°C, the pore size increased as the NC content and the sintering temperature increased. The thermal conductivity was maintained at less than 0.28 W/m‧K. Therefore, it is possible to use 6-8 wt% NC as a blowing agent in glass material to produce foamed glass that has closed pores of approximately 500 µm with better or equivalent compressive strength and thermal conductivity properties than existing 1000 µm grade foamed glass, despite being sintered at a temperature of approximately 100°C lower.
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