Effects of follicle-stimulating hormone on the proliferation and apoptosis of infantile hemangioma stem cells.

Objective: To investigate the effects of different concentrations of follicle-stimulating hormone (FSH) on the proliferation and apoptosis of human hemangioma stem cells, it will provide a basis for studying the mechanism of FSH in treating hemangioma. Methods: Hemangioma specimens were collected from the Longgang District Maternity & Child Healthcare Hospital of Shenzhen City. Hemangioma stem cells were treated with different concentrations of FSH. Cell viability was detected by CCK8 method and cell apoptosis was analyzed by flow cytometry. Results: Hemangioma stem cells (HemSCs) were extracted from fresh tissue of infantile hemangioma by the CD133 immunomagnetic bead method. Under the influence of FSH at different concentrations (0, 100, 1000 IU/L), the cell viability of hemangioma stem cells increased significantly in a concentration-dependent manner (P < 0.05). At the same time, the apoptosis of hemangioma stem cells decreased with increasing concentrations of follicle-stimulating hormone (P < 0.05). Specifically, 1000 IU/L FSH significantly promoted the proliferation of hemangioma stem cells and inhibited their apoptosis. Conclusion: High concentration of follicle-stimulating hormone can maintain the growth of hemangioma by promoting the proliferation and inhibiting the apoptosis of hemangioma stem cells.

Comprehensively Analyze the Prognosis Significance and Immune Implication of PTPRO in Lung Adenocarcinoma.

Immunotherapy for lung adenocarcinoma (LUAD) is considered to be a promising treatment option, but only a minority of patients benefit from it. Therefore, it is essential to clarify the regulation mechanism of the tumor immune microenvironment (TIM) of the LUAD. Receptor-type protein tyrosine phosphatase (PTPRO) has been shown to be a tumor suppressor in a variety of tumor; however, its role in LUAD has never been reported. In this study, we first found that PTPRO was lowly expressed in LUAD and positively correlated with patient prognosis. Next, we investigated the relationship between PTPRO and clinical characteristics, and the results showed that gender, age, T, and stage were closely related to the expression level of PTPRO. Moreover, we performed univariate and multivariate analyses, and the results revealed that PTPRO was a protective factor for LUAD. By constructing a nomogram based on the expression level of PTPRO and various clinical characteristics, it was proved that the nomogram has a good predictive capacity. Furthermore, we analyzed the coexpression network of PTPRO through multiple databases and performed GO and KEGG enrichment analyses. The results demonstrated that PTPRO was involved in the regulation of multiple immune pathways. In addition, we analyzed whether PTPRO expression of LUAD regulate immune cell infiltration and the results demonstrated that PTPRO was closely related to the infiltration of various immune cells. Finally, we predicted LUAD sensitivity to chemotherapeutics and response to immunotherapy by PTPRO expression levels. The results showed that PTPRO expression level affect the sensitivity of various chemotherapeutic drugs and may be involved in the efficacy of immunotherapy. These results we obtained suggested that PTPRO is closely related to the prognosis and TIM of LUAD, which may be a potential immunotherapeutic target for LUAD.

Association Between an Interferon Regulatory Factor 6 Gene Polymorphism and Nonsyndromic Cleft Palate Risk.

Background: Involvement of interferon regulatory factor 6 (IRF6) gene polymorphisms in nonsyndromic cleft palate (NSCP) risk remains controversial. This investigation was performed to evaluate the relationship between IRF6 gene polymorphisms and NSCP risk. Materials and Methods: Two hundred forty-one patients with NSCP (including 103 complete trio families) were recruited, and 242 unaffected individuals were included as controls. Polymorphisms for the IRF6 rs2235371, rs801619, rs642961, rs44844880, and rs8049367 loci were characterized in both groups. Furthermore, eligible studies were identified from the databases through June 1, 2017, and were included in a meta-analysis to enhance the robustness of our conclusions. Results: The IRF6 rs2235371 A allele and AA genotype in the case group were found at higher frequencies than in the control group (A allele: p < 0.0016; AA genotype: p < 0.0049). The IRF6 rs801619 AA genotype and G allele were associated with NSCP risk (G allele: p < 0.0061; AA genotype: p < 0.0195). At the IRF6 rs642961, rs44844880, and rs8049367 loci genotype and allele frequencies were not statistically different between the NSCP group and normal controls. In the meta-analysis, the IRF6 A/G gene polymorphism (rs2235371) and IRF6 A/G gene polymorphism (rs642961) were associated with NSCP risk in the general population, whereas the IRF6 A/C gene polymorphism (rs2013162) was not. Conclusion: The IRF6 A/G gene polymorphisms at rs2235371 and rs642961, but not the IRF6 A/C gene polymorphism rs2013162, were associated with NSCP risk.