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Background The functionality of lncRNA snaR has only been characterized in breast cancer and colon cancer. The aim of the current study is to explore the involvement of lncRNA snaR in ovarian carcinoma (OC). Materials and methods Expression of lncRNA snaR and GRB2-associated binding protein 2 (GAB2) in plasma of both patients with OC and healthy females was detected by qRT-PCR. Application value of plasma lncRNA snaR in the diagnosis of OC was evaluated by ROC analysis. Correlation between plasma lncRNA snaR and GAB2 was analyzed by Pearson correlation coefficient. LncRNA snaR and GAB2 expression vectors as well as GAB2 siRNA were transfected into cells of human OC cell lines, and the effect on lncRNA snaR expression, GAB2 expression and cell proliferation was detected by qRT-PCR, western blot and CCK-8 assay. Results It was observed that plasma levels of lncRNA snaR and GAB2 were significantly higher in OC patients than those in healthy controls. In effect, high levels of plasma lncRNA snaR and GAB2 distinguished OC patients from healthy controls. Plasma lncRNA snaR and GAB2 were positively correlated in OC patients but not in healthy controls. LncRNA snaR overexpression promoted cancer cell proliferation and upregulated GAB2 expression. Conclusions GAB2 overexpression also promoted cancer cell proliferation but showed no significant effects on lncRNA snaR expression, while GAB2 siRNA silencing significantly attenuated the enhancing effects of lncRNA snaR overexpression on cancer cell proliferation. LncRNA snaR may promote proliferation of ovarian carcinoma cells by upregulating GAB2 expression. [ABSTRACT FROM AUTHOR]

HSP60 has been proved to be closely related to atherosclerosis due to its antigenicity. To determine this antigenicity effect, the ApoE−/− mice were fed with western-type diet and HSP60 was administrated orally or subcutaneously (SC) for potential vaccine against atherosclerosis. Here, we observed the ApoE−/− mice with oral HSP60 administration group showed a significant reduction in plaque size at the aortic root; accompanied by increased MSDCs (CD11b + Gr1 + ) in peripheral blood and spleen which was mostly composed of M-MDSCs (CD11b + LY6G − LY6C high ), and increased plasma IL-10 and splenic Foxp3, Arg1, iNOS mRNA as well as decreased plasma IFN-γ and splenic T-bet mRNA compared to control group. Surprisingly, ApoE−/− mice with subcutaneous HSP60 administration group showed contrary results and their MDSCs were mostly composed of G-MDSCs (CD11b + LY6G + LY6C low ). As expected, both PBS-oral and PBS-SC groups showed no significant effects on both the immune response and atherosclerotic plaque formation. In contrast, subcutaneous administration of HSP60 causes the opposite response. Thus, we propose the proper method for administering HSP60 as a new immunologic agent for prevention and treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Cyclin D1 (CCND1) has been identified as a metastatic promoter in various tumors including lung adenocarcinoma (LUAD), a subtype of non small cell lung cancer (NSCLC). The previous observation revealed that CCND1 was upregulated in NSCLC and predicted poor prognosis of LUAD patients. In this study, we examined a chaperonin containing TCP1 subunit 5 (CCT5) protein interacts with CCND1 in LUAD. Immunofluorescence demonstrated the co-localization of CCT5 and CCND1 protein in LUAD cells. CCT5 expression was detected with both immunohistochemistry (IHC) and bioinformatics analyses. Similar with the expression pattern of CCND1, CCT5 displayed a high level in LUAD tissues compared to non cancerous lung specimens. Patients with high CCT5 expression showed a significant shorter overall survival relative to those with low expression level. Furthermore, upregulated CCT5 exhibited significant positive correlation with TNM stage of LUAD patients in both IHC analyses and bioinformatics. Knocking down CCT5 remarkably inhibited LUAD cell migration and invasion in vitro by inactivating PI3K/AKT and its downstream EMT signals, which could abrogated the accelerated migration and invasion caused by CCND1 overexpression. In summary, our study discovered a highly expressed protein CCT5 in LUAD which interacted with CCND1 and promoted migration and invasion of LUAD cells by positively moderating PI3K/AKT-induced EMT pathway. ∙ CCT5 functions as a role for promoting tumor progression. ∙CCT5 interacts with CCND1 to promote the migration and invasion of lung carcinoma. ∙Patients with high CCT5 expression showed a poor overall survival prognosis. [ABSTRACT FROM AUTHOR]