Conflicting results were implicated in both single case-control studies and meta-analyses of the correlation between p73 G4C14-to-A4T14 polymorphism and lung cancer risk. We designed this study to further assess the association by meta-analysis. A meta-analysis was performed based on five case-control studies (5,467 subjects) retrieved from PubMed and Embase. Odds ratios (ORs) with 95 % confidence intervals (CIs) were measured for the association using the models of random effects and fixed effects. The results showed no evidence between p73 G4C14-to-A4T14 polymorphism and lung cancer risk in any genetic model (allele model: OR, 1.06, 95 % CI, 0.89-1.26; homozygote genotypes: OR, 1.18, 95 % CI, 0.80-1.73; heterozygote genotypes: OR, 1.04, 95 % CI, 0.89-1.23; dominant model: OR, 1.05, 95 % CI, 0.89-1.24; recessive model: OR, 1.17, 95 % CI, 0.93-1.47). Subgroup analyses according to ethnicity, however, detected significant association in Caucasian population. Our study provides evidence that p73 G4C14-to-A4T14 polymorphism may play a major role in susceptibility to lung cancer in Caucasians.

Chronic obstructive pulmonary disease is the 3rd leading cause of death worldwide, and the available treatments are unsatisfactory, resulting in a major economic burden. As cellular therapy is commonly used for lung disease, we investigated a treatment with CXCR4-overexpressing BMSCs in a COPD model. We extracted and purified Bone marrow mesenchymal stem cells (BMSCs) from SD rats. COPD apoptosis model was established by cigarette smoke exposure. BMSCs (1 × 10 6 cells per injection)were transplanted in vivo twice a month during model establishment, and alveolar rupture in the lung was assessed. Lung cell apoptosis was assessed by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) analysis, and the concentrations of apoptotic proteins in the lungs were detected by Western blotting. We successfully isolated BMSCs and established CXCR4-overexpressing BMSCs. qRT‒PCR and Western blotting detection both reveal that CXCR4 mRNA level and protein both significantly higher expression in CXCR4-BMSCs than the pBABE-BMSCs. Continuous cigarette smoke exposure caused alveolar septal rupture: In the model group, the alveolar mean linear intercept in the first month was significantly lower than that in the third month ( p < 0.05). In the third month, the alveolar mean linear intercept values of the control and CXCR4-BMSC groups were lower than those of the model group (control group p < 0.01, CXCR4-BMSC group p < 0.05), and TUNEL staining revealed that the apoptosis rates of the control and CXCR4-BMSC groups were significantly lower than those of the model group ( p < 0.01). Furthermore, the levels of the apoptotic proteins cleaved caspase-8, cleaved caspase-3 and cleaved PARP-1 were higher in the model group than in the control group ( p < 0.05) and significantly lower in the CXCR4-BMSC group than in the model group ( p < 0.05). The transplantation of CXCR4-overexpressing BMSCs during COPD model generation significantly inhibited apoptosis via the extrinsic apoptosis pathway. Graphical abstract CXCR4 enhances the inhibitory effects of bone mesenchymal stem cells on lung cell apoptosis in a rat model of smoking-induced COPD

Objective Chronic obstructive pulmonary disease (COPD) is the 3rd leading cause of death worldwide, and treatments are unsatisfactory, resulting in a major economic burden. Cellular therapy is commonly used for lung disease. We investigated treatment with CXCR4-overexpressing BMSCs during COPD model establishment. Methods We extracted and purified BMSCs from SD rats. Apoptosis induced by COPD was established by cigarette smoke exposure. BMSCs were transplanted in vivo twice a month during model establishment, and alveolar rupture in the lung was assessed. Lung cell apoptosis was assessed by TUNEL analysis, and the concentrations of apoptotic proteins in the lungs were detected by Western blotting. Results We successfully isolated BMSCs and established CXCR4-overexpressing BMSCs. Continuous cigarette smoke exposure caused alveolar septal rupture: in the model group, the 1-month alveolar MLI was significantly lower than that at the third month (p < 0.05). In the third month, the alveolar MLIs of the control and CXCR4-BMSC groups were lower than those of the model group (control group p < 0.01, CXCR4-BMSC group p < 0.05), and as shown by TUNEL staining, the apoptosis rates of the control and CXCR4-BMSC groups were significantly lower than those of the model groups (p < 0.01). The levels of the apoptotic proteins cleaved caspase-8, cleaved caspase-3 and cleaved PARP-1 were higher in the model group than in the control group (p < 0.05) and significantly lower in the CXCR4-BMSC group than in the model group (p < 0.05). Conclusion Transplantation of CXCR4-overexpressing BMSCs during COPD model generation significantly inhibited apoptosis via the extrinsic apoptosis pathway.

Acute myeloid leukemia remains a therapeutic challenge in the medical field and improvement in chemotherapeutics is needed. In this paper, MOLM-13 cells were treated with different concentrations (0, 10, 50, 100 µM) of dentatin and cell viability was detected using Cell Counting Kit-8. Cell cycle and cell apoptosis rates were evaluated by flow cytometry. The relevant proteins were assessed by Western blot. Consequently, the results show that dentatin inhibits the cell viability in a dose-dependent manner. In addition, dentatin arrests the cell cycle at G1 phase (P ‹ 0.01). Moreover, dentatin induces the cell apoptosis. Further study revealed that dentatin downregulates the phosphorylated STAT3 and CyclinD1 but upregulates the cleaved caspase-3. In summary, this study confirms that dentatin inhibits MOLM-13 cell viability, increases cell apoptosis, and retards cell cycle.