BackgroundNIPBL, the sister chromatid cohesion 2 (SCC2) human homolog, is a cohesin loading factor which is essential for deposition of cohesin onto the sister chromatid. Recent studies have shown that NIPBL contribute to sister chromatid cohesion and plays a critical role in development, DNA repair, and gene regulation. In this study, we measured the expression of NIPBL in clinical non-small cell lung cancer specimens, and determined its effects on cellular processes and chemosensitivity in vitro.MethodsNIPBL immunohistochemistry was performed on 123 lung adenocarcinoma samples. Through knockdown of NIPBL protein expression, non-small cell lung cancer cell lines were used to test the potential involvement of NIPBL silencing on cell proliferation, migration, invasion, and apoptosis. Chemosensitivity was assessed with clonogenic assays, and chromatin immunoprecipitation assays were performed to analyze the relationship between NIPBL and signal transducers and activators of transcription 3 (STAT3).ResultsImmunohistochemical analysis showed that high expression of NIPBL was strongly correlated with poor prognosis, tumor differentiation, and lymph node metastasis. Survival analysis further indicated that NIPBL expression was a potential prognostic factor for non-small cell lung cancer. Knockdown of NIPBL in non-small cell lung cancer cell lines significantly reduced cellular proliferation, migration, and invasion, and enhanced cellular apoptosis and sensitivity to cisplatin, paclitaxel, and gemcitabine hydrochloride. NIPBL bound to the promoter region of the STAT3 gene, directly regulating the expression of STAT3.ConclusionsThese data suggested that NIPBL played a significant role in lung carcinogenesis. NIPBL expression conferred poor prognosis and resistance to chemotherapy in non-small cell lung cancer, suggesting that NIPBL may be a novel therapeutic target.

Objective. To observe the inhibitory effect of solanine on regulatory T cells (Treg) in transplanted hepatoma mice and to study the mechanism of solanine inhibiting tumor growth. Methods. The levels of Treg cells and IL-2, IL-10, and TGFβ in the blood of patients with liver cancer were detected by flow cytometry and ELISA, respectively. A mouse hepatocellular carcinoma (HCC) graft model was established and randomly divided into four groups: control group, solanine group, TGFβ inhibitor group (SB-431542), and solanine +TGFβ inhibitor combined group. Tumor volume of each group was recorded, tumor inhibition rate was calculated, and tumor metastasis was counted. The proportion of CD4+CD25+Foxp3+ Treg in transplanted tumor tissues was detected by flow cytometry. The expression levels of Foxp3 and TGFβ in transplanted tumor tissues were detected by quantitative fluorescence PCR. Results. Compared with healthy people, Treg cells and IL-2, IL-10, and TGFβ contents in peripheral blood of liver cancer patients were increased. The results of the transplanted tumor model in mice showed that the tumor volume of the transplanted mice in the solanine group and the TGFβ inhibitor mice was reduced compared with the control group. The combined group had the smallest tumor volume. The proportion of CD4+CD25+Foxp3+ Treg in the transplanted tumor tissues of mice in the solanine treatment group was significantly lower than that in the control group. The expressions of Foxp3 and TGFβ in the transplanted tumor tissues of mice in the solanine group were significantly lower than those in the control group. Conclusion. Solanine may enhance the antitumor immune response by downregulating the proportion of CD4+CD25+ Treg and the expression of Foxp3 and TGFβ in tumor tissues.

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Interleukin polymorphisms might influence predisposition to lung cancer (LC), but the results of already published studies regarding the relationship between interleukin polymorphisms and LC were still controversial and ambiguous. So the authors designed this meta‐analysis to more precisely estimate relationship between interleukin polymorphisms and LC by pooling the results of already published related studies. The authors searched Pubmed, Embase, Web of Science, and CNKI for already published studies. Thirty‐five already published studies were pooled and analyzed in this meta‐analysis. The pooled meta‐analyses results showed that distributions of IL‐4 rs2243250 polymorphism among patients and controls from Asian countries differed significantly (dominant comparison: OR = 1.29, 95% CI 1.07–1.55; overdominant comparison: OR = 0.83, 95% CI 0.73–0.95; allele comparison: OR = 1.26, 95% CI 1.03–1.54), and distributions of IL‐10 rs1800872 polymorphism among patients and controls from Caucasian countries also differed significantly (recessive comparison: OR = 0.54, 95% CI 0.35–0.83; overdominant comparison: OR = 1.26, 95% CI 1.05.1.51). No genotypic distribution differences were observed for IL‐4 rs2070874, IL‐6 rs1800795, IL‐6 rs1800796, IL‐8 rs4073, IL‐10 rs1800871, and IL‐10 rs1800896 polymorphisms in pooled meta‐analyses. This meta‐analysis suggested that IL‐4 rs2243250 might influence predisposition to LC in Asians, whereas IL‐10 rs1800872 polymorphism might influence predisposition to LC in Caucasians.