Identification of candidate target genes of genomic aberrations in esophageal squamous cell carcinoma

Abstract

Abstract. The aim of the present study was to identify the candidate target genes of genomic aberrations in esophageal squamous cell carcinoma (ESCC). Array comparative genomic hybridization (CGH) and quantitative polymerase chain reaction were applied to analyze the copy number changes and expression level of candidate genes, respectively. Integrative analysis revealed that homozygous deletions of cyclin-dependent kinase inhibitor (CDKN) 2A and CDKN2B and gains of fascin actin-bundling protein 1 (FSCN1) and homer scaffolding protein 3 (HOMER3) occurred frequently in ESCC. The results demonstrated that the homozygous deletion of CDKN2A or CDKN2B was significantly associated with lymph node metastasis. Notably, the expression of CDKN2A and CDKN2B was lower in dysplasia than in normal esophageal epithelium. We also observed that the copy number increase of FSCN1 was significantly associated with pT, pN and pStage, and that the gain of HOMER3 was significantly linked with pN and pStage. We further revealed that FSCN1 and HOMER3 were overexpressed in ESCC, and that their overexpression was correlated with copy number increase. In conclusion, CDKN2A, CDKN2B, FSCN1 and HOMER3 are candidate cancer-associated genes and may play a tumorigenic role in ESCC.

Expression of tumor growth related genes in IRE1 knockdown U87 glioma cells: effect of hypoxia

“…Therefore, our results concerning strong down-regulation of COL6A1 gene expression in glioma cells upon inhibition of IRE1 completely agree with the functional role of this protein in tumor cells and with suppression of IRE1 knockdown glioma cell proliferation [7,22]. We have also shown that the expression of DEK, HOMER3, and GNPDA1 genes is downregulated and these results agree well with data concerning the functional role of DEK, HOMER3, and GNPDA1 proteins encoding by these genes [25][26][27]. Thus, DEK induces cell proliferation and its expression is required for tumorigenesis [25]; HOMER3 is overexpressed in some cancers [26], and GNPDA1 enhances cell proliferation through the synthesis of glycoconjugates and modification of intracellular proteins [27].…”

“…BCL2L1 (BCL2-like 1), a nuclear gene encoding apoptosis regulator, which represents regulatory subunit 52 of protein phosphatase 1, plays an important role in both positive and negative regulation of programmed cell death. Recently, it was shown that HOMER3 is overexpressed in some cancers and possibly related to tumor growth [26]. Glucosamine-6-phosphate deaminase (GNPDA1) catalyzes the reversible conversion of D-glucosamine-6-phosphate into D-fructose-6-phosphate and plays a key role in the maintenance of UDP-N-acetylglucosamine, which is a glucose metabolite with pivotal functions as a key substrate for the synthesis of glycoconjugates like hyaluronan, and as a metabolic sensor that controls cell functions through modification of intracellular proteins [27].…”

“Biological Adhesion” is a Significantly Regulated Molecular Process during Long-Term Primary In Vitro Culture of Oviductal Epithelial Cells (Oecs): A Transcriptomic and Proteomic Study

“…Apart from the abovementioned genes and their products, we also selected a group with known function in adhesion process but without proven role in reproduction, including: fascin actin bundling protein 1 (FASCN1) [63,64,65,66,67], myosin light chain 1 (MYL9) [68], caldesmon 1 (CALD1) [69], and hemoglobin subunit beta (HBB) [70]. Further examination may explain their yet unrevealed potential in reproduction.…”

HOMER3 facilitates growth factor-mediated β-Catenin tyrosine phosphorylation and activation to promote metastasis in triple negative breast cancer

“…Notably, a recent report indicates that genomic amplification contributes to HOMER3 overexpression in esophageal squamous cell carcinoma [ 24 , 36 ]. However, no significant copy number alteration of the HOMER3 genomic locus could be observed from the TCGA breast cancer dataset [ 11 ].…”