Abildgaardpittman4846

Ingenuity Pathway Analysis to show that KDELR2 has a significant impact in canonical pathway in cell cycle regulation and participate in multiple pathways. And we detected the cell cycle proteins CCND1 expression by Western blot analysis. Results Our results showed that KDELR2 was up-regulated in glioma tissue and cell lines. Knockdown KDELR2 was able to reduce cell viability, promote cell cycle arrest at the G1 phase, and induce apoptotic cell death. Moreover, our results suggested that KDELR2 regulated the cellular functions of U87 cells by targeting CCND1. Therefore, we demonstrated that KDELR2 is a novel biomarker in glioma. Conclusions KDELR2 is highly expressed in human glioma tissues and cell lines, a higher expression of KDELR2 is associated with a poor prognosis of glioma patients. NF-κΒ activator 1 mouse Moreover, KDELR2 regulated the cellular functions of U87 cells by targeting CCND1. The KDELR2/CCND1 axis may provide a new therapeutic target for the treatment of glioma and deepen our understanding of glioma mechanisms.Breast cancer (BC) is the most frequent tumor in women and genetic factors are among the main risk factors contributing to this malignancy. Chromosome 9p21 contains important regulatory non-coding RNAs and is associated with multiple malignancies including BC. The current meta-analysis aimed to investigate the association between genetic variants within the 9p21 locus and risk of breast cancer. A literature search was performed using PubMed, Web of Science, Embase, MEDLINE, Scopus and Clinical key databases. Nine studies containing 23,726 subjects were eligible for the final analysis and specific odds ratios (OR) and confidence intervals (95% CI) were evaluated to assess the strength of the associations. In the pooled analysis, there was an association between the genetic variations in 9p21 locus (CDKN2A/2B) with risk of breast cancer with a standard OR of 1.22 (95% CI 1.04-1.45, P = 0.016; random-effects model), supporting the significance of this locus as a novel risk factor for breast cancer patients. In conclusion, our results showed that 9p21 region is positively associated with risk of BC and its polymorphisms may be a candidate marker for BC susceptibility.Background miR-194-5p has been associated with drug resistance in many cancers. However, the role of miR-194-5p in cisplatin resistance in ovarian cancer is still unclear. Materials and methods To study the role and mechanism of miR-194-5p in cisplatin resistance, qRT-PCR was performed to determine the expression of miR-194-5p and SLC40A1 in ovarian cancer. Cell Counting Kit-8 (CCK8) assay was used to analyse cell viability after cisplatin treatment. Dual-luciferase reporter gene assay was performed to examine the relationship between miR-194-5p and SLC40A1. The genes downstream of SLC40A1 were investigated through bioinformatics analysis. Results Compared to cisplatin-sensitive ovarian cancer cells, higher miR-194-5p expression and lower SLC40A1 expression were found in cisplatin-resistant ovarian cancer cells. Moreover, this study demonstrated that over-expression of miR-194-5p inhibited SLC40A1 expression, and knockdown of miR-194-5p promoted SLC40A1 expression. In addition, dual-luciferase reporter gene acould be a potential therapeutic target and a prognostic biomarker for ovarian cancer, with important implications for future research.Background Increasing studies highlight the crucial role of long non-coding RNAs (lncRNAs) in carcinogenesis of various human cancer types, including esophageal cancer (ESCA). Long intergenic non-coding RNA 00460 (Linc00460), a novel oncogenic lncRNA, has been reported to accelerate ESCA cell growth. This study aimed to investigate the role and possible regulatory mechanism of linc00460 in ESCA metastasis. Methods Bioinformatics analysis and quantitative real time polymerase chain reaction (qRT-PCR) were used to detect linc00460 expression in ESCA. Wound healing assay, Transwell assay and Western blot were utilized to examine migration, invasion and epithelial-mesenchymal transition (EMT) of ESCA cells. The direct binding effect between linc00460 and microRNA-1224-5p (miR-1224-5p) was evaluated by the dual luciferase reporter assay. Results In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines. Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells. In addition, miR-1224-5p, a potential tumor suppressor, was negatively correlated with linc00460 in ESCA. Linc00460 and miR-1224-5p could bind directly in ESCA cells. Inhibition of miR-1224-5p partially abrogated the effects of linc00460 decrease on metastatic potential and EMT of ESCA cells. Conclusions Taken together, linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. Our findings suggest that linc00460/miR-1224-5p is a possible clinical target for ESCA.Background Cyclin-dependent kinase 12 (CDK12) belongs to the cyclin-dependent kinase (CDK) family, modulating multiple cellular functions including DNA damage response (DDR), development and cellular differentiation, transcription, mRNA processing, splicing and pre-mRNA processing. CDK12 has been reported as both tumor suppressor and oncogene in various kinds of tumor. The function of CDK12 in gastric cancer (GC) remains unclear. Methods/results CDK12 mRNA expression was decreased in GC compared with non-tumor tissue based on GEO database. Also, low mRNA expression of CDK12 was detected in GC cell lines by qPCR. Similarly, CDK12 protein expression was also reduced in GC tissues compared with adjacent non-tumor tissues in 177 GC patients as shown by immunohistochemistry. Low expression of CDK12 was associated with organ metastasis, poorly differentiated adenocarcinoma and advanced stage. Consistent with human protein atlas database analysis, Low expression of CDK12 was correlated with worse overall survival (P less then 0.001). Multivariate Cox regression indicated that low expression of CDK12 was an independent prognostic factor for GC patients (P less then 0.001). Finally, a gene set enrichment analysis was performed to detect underlying internal mechanisms and biological processes. Conclusions CDK12 is down-regulated in GC and its expression is negatively correlated with advanced stage, poorly differentiated adenocarcinoma and poor outcomes. Our findings suggest that CDK12 may be a potential tumor suppressor in GC.