Anti-CENPF (aa 2350-2450) polyclonal antibody

Adenoid cystic carcinoma (ACC) is one of the most frequent malignancies of salivary glands. The objective of this study was to identify key genes and potential mechanisms during ACC samples. The gene expression profiles of GSE88804 data set were downloaded from Gene Expression Omnibus. The GSE88804 data set contained 22 samples, including 15 ACC samples and 7 normal salivary gland tissues. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were constructed, and protein-protein interaction network of differentially expressed genes (DEGs) was performed by Cytoscape. The top 10 hub genes were analyzed based on Gene Expression Profiling Interactive Analysis. Then, DEGs between ACC samples and normal salivary gland samples were analyzed by gene set enrichment analysis. Furthermore, miRTarBase and Cytoscape were used for visualization of miRNA-mRNA regulatory network. KEGG pathway analysis was undertaken using DIANA-miRPath v3.0. In total, 382 DEGs were identified, including 119 upregulated genes and 263 downregulated genes. GO analysis showed that DEGs were mainly enriched in extracellular matrix organization, extracellular matrix, and calcium ion binding. KEGG pathway analysis showed that DEGs were mainly enriched in p53 signaling pathway and salivary secretion. Expression analysis and survival analysis showed that ANLN, CCNB2, CDK1, CENPF, DTL, KIF11, and TOP2A are all highly expressed, which all may be related to poor overall survival. Predicted miRNAs of 7 hub DEGs mainly enriched in proteoglycans in cancer and pathways in cancer. This study indicated that identified DEGs and hub genes might promote our understanding of molecular mechanisms, which might be used as molecular targets or diagnostic biomarkers for ACC.

Basal-like breast cancer (BLBC) is resistant to endocrinotherapy and targeted therapy and new molecular therapies are needed for BLBC. In this study, we evaluated the role of DUSP1 and DUSP5, negative regulators of mitogen-activated protein kinase pathway, in the aggressiveness of BLBC. MDA-MB-231 cells were given paclitaxel (PTX) treatment and subsequently PTX resistant cell clones were established. Microarray analysis, real-time quantitative reverse transcription PCR (qRT-PCR), and online analysis of large cohorts of breast cancer patients were performed. The PTX resistant cells showed stronger cell proliferation ability by exhibiting the upregulation of CENPF, CDC6, MCM3, CLSPN and SMC1A expression. Furthermore, DUSP1 and DUSP5 expression was significantly downregulated in PTX resistant cells. In addition, in large breast cancer patients' database, both DUSP1 and DUSP5 correlated negatively with higher histological grade. DUSP1 low expression was obvious in HER2 positive and basal like while DUSP5 low expression was peculiar for basal like compared with other subtypes. Remarkably, low expression of DUSP5, but not DUSP1, was significantly correlated with poor survival of BLBC patients. In conclusion, our data suggest that loss of DUSP5 expression results in PTX resistance and tumor progression, providing a rationale for a therapeutic agent that restores DUSP5 in BLBC.