Anti-CDH2 monoclonal antibody, clone 3H8

BackgroundOvarian cancer (OC) is the most malignant tumor in the female reproductive system. About 75% of OC in complete remission of clinical symptoms still develop a recurrence. Therefore, searching for new treatment methods plays an important role in improving the prognosis of OC.MethodsWe downloaded the MAF files, RNA-seq data and clinical information from the TCGA database. The "maftools" package in R software was used to visualize the OC mutation data. We calculated the tumor mutation burden (TMB) of OC and analyzed its correlation with clinicopathological parameters and prognostic value. Tumor mutation burden related signature model was constructed to predict the overall survival (OS) of OC.ResultsThe results revealed that there was a statistical correlation between TMB and FIGO stage, grade and tumor residual size of ovarian cancer patients. The Kaplan-Meier curve indicated that a high TMB is associated with better clinical outcomes of OC. The difference analysis indicated 24 upregulated genes and 619 downregulated genes in the high-TMB group compared with the low-TMB group. Besides, the TMBRS model based on five hub genes (RBMS3, PLA2G5, CDH2, AMHR2 and ADAMTS8) was constructed to predict the OS of OC. The ROC curve and validation data sets all revealed that the TMBRS model was reliable in predicting recurrence risk. Immune microenvironment analysis indicated the correlations between TMB and infiltrating immune cells.ConclusionsOur results suggest that TMB plays an important role in the prognosis and guiding immunotherapy of OC. By detecting the TMB of OC, clinicians can more accurately treat patients with immunotherapy, thereby improving their survival rate.

Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 mu M for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and anti metastatic activity of SA.