Anti-TBPL1 (aa 114-135) polyclonal antibody

Recent advances in the understanding of microRNA have rendered microRNAs (miRNAs) a compelling novel class of biomarker in cancer biology. However, the specific function of miRNA-18a (miR-18a) in colorectal cancer (CRC) remains unclear. In the present study, the role of miR-18a in the carcinogenesis of CRC was investigated. miR-18a expression was assessed in CRC specimens and cell lines using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The targets of miR-18a were predicted using bioinformatics tools. Luciferase reporter assays were used to confirm the functional association between miR-18a and its target genes. The effect of miR-18a on cell proliferation, invasion and migration was confirmed in vitro by a methylthiazol tetrazolium assay, cell invasion assay, and wound healing assay. Gene and protein expression was examined using RT-qPCR and western blotting, respectively. It was demonstrated that the expression of miR-18a in CRC tissues and cell lines was markedly lower than in normal control tissues and cells, respectively. In addition, miR-18a inhibited cell proliferation, invasion and migration in CRC cells. Moreover, TATA box-binding protein-like protein 1 (TBPL1) was identified as a potential target gene of miR-18a in the bioinformatics analysis and luciferase reporter assays, and miR-18a directly inhibited TBPL1 expression by targeting its 3'-untranslated region. Furthermore, TBPL1 was downregulated and inversely correlated with miR-18a expression in tissues. These findings demonstrate that miR-18a exhibits a protective role in CRC via inhibiting proliferation, invasion and migration of CRC cells by directly targeting the TBPL1 gene.

In this study, we aimed to identify genes that could be involved in alternative pathways linked to the pathogenesis of non-small cell lung cancer (NSCLC), which could provide novel molecular biomarkers. Owing to NSCLC subtypes, three individual NSCLC data sets were downloaded and analyzed. Gene-subsetting subsequent meta-analysis was performed to screen differentially expressed genes (DEGs). The functional enrichment and pathway analyses were then executed using comprehensive bioinformatics analysis. Accordingly, the three hub genes of alternative pathways and their strong correlation with NSCLC pathway were initially identified as potential candidates (common DEGs) for the progression of NSCLC. The clinicopathological functions of common DEGs in NSCLC were validated by analyzing transcription factors targeting common DEGs, and their effectiveness was validated by analysis of protein/gene interactions and biological processes annotations. Finally, elucidated genes, such as protein phosphatase 3 catalytic subunit alpha (PPP3CA) of calcium signaling pathway, ubiquitin conjugating enzyme E2-Q1 (UBE2Q1) of beta-catenin-EGFR-PI3K-Akt-mTOR signaling pathway and TATA-Box binding protein like-1 (TBPL1) of RNA polymerase-II transcription initiation and promoter clearance and PI3K-Akt signaling pathway were recognized as alternative networks mostly associated with the progression of NSCLC by co-occurred with oncogenes of the extracellular-signal-regulated kinase (ERK) pathway; and these genes can confer resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in NSCLC therapy through various mechanisms. Together, these results indicate that mutation-activated alternative pathway genes and related checkpoints can confer progression to NSCLC and drug resistance; therefore, which could provide as promising biomarkers for early detection and treatment of NSCLC.