On MDCT, ground-glass opacities and areas of consolidation had a predominant peribronchovascular and subpleural distribution, resembling organising pneumonia;
they progressed to bilateral extensive airspace disease in severely ill patients.”
“Background: Glycogen synthase kinase 3 beta (GSK3 beta) is centrally involved in diverse cellular processes, including proliferation and apoptosis. This study aimed to investigate the influence of GSK3 beta expression on the prognosis of human non-small cell lung cancer (NSCLC) and the effects of GSK3 beta inhibition in NSCLC cell lines. Methods: Immunohistochemical and western blot assays were used to GSK126 evaluate the GSK3 beta expression level in human NSCLC tissues. Lentiviral RNA interference was performed to inhibit the expression of GSK3 beta in the A549,
H292, H1299 and SK-MES-1 cell lines. Cell survival, apoptosis and motility were evaluated in vivo and in vitro. Results: The levels of GSK3 beta were greater in NSCLC tissues (n = 211) than in control tissues (n = 194) (P smaller than 0.001). The 5-year follow-up analysis showed that positive GSK3 beta expression was indicative of poor prognosis (P = 0.006). Furthermore, knockdown of GSK3 beta in NSCLC cell lines suppressed cell proliferation, arrested tumor cells in G0/G1 phase, induced apoptosis and reduced cell motility. A xenograft model showed that the deregulation of GSK3 beta attenuated tumorigenesis, as confirmed by reduced cell proliferation based on
Ki-67 and significantly increased apoptotic cell death. The inhibition of GSK3 beta had inconsistent effects on PKC412 the expression of beta-catenin, depending on the cell type examined. Conclusion: Aberrant expression of GSK3 beta serves as an independent marker of poor prognosis for NSCLC. The inhibition of GSK3 beta suppressed tumorigenesis by attenuating cell proliferation, increasing apoptosis and restraining cell selleck chemicals motility. These results identify GSK3 beta as a tumor promoter and a potential therapeutic target in NSCLC.”
“Insulin-like growth factor binding protein 7 (IGFBP7) has been shown to be a tumor suppressor in a variety of cancers. We previously have shown that IGFBP7 expression is inversely correlated with disease progression and poor outcome in breast cancer. Overexpression of IGFBP7 in MDA-MB-468, a triple-negative breast cancer (TNBC) cell line, resulted in inhibition of growth and migration. Xenografted tumors bearing ectopic IGFBP7 expression were significantly growth-impaired compared to IGFBP7-negative controls, which suggested that IGFBP7 treatment could inhibit breast cancer cell growth. To confirm this notion, 14 human patient primary breast tumors were analyzed by qRTPCR for IGFBP7 expression. The TNBC tumors expressed the lowest levels of IGFBP7 expression, which also correlated with higher tumorigenicity in mice.