Long noncoding RNA LSINCT5 is up-regulated and related to progression in esophageal squamous cell carcinoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE128035 | GEO | 2022/03/07
REPOSITORIES: GEO
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Project description:Esophageal squamous cell carcinoma (ESCC) is characterized as a metabolic disorder characterized by lipid metabolic reprogramming. To investigate the regional characteristics of ESCC patients in Xinjiang Province, China, and lipid metabolism, in this study, we described the characteristics of the serum lipid composition in Kazakh ESCC patients by performing an integrated analysis of the transcriptome and lipidomic data. Serum samples from 30 Kazakh ESCC patients and 30 healthy individuals were subjected to targeted lipid metabolomics analysis via UPLC‒MS/MS, while 3 tumor samples and matched adjacent normal tissues from 30 ESCC patients were subjected to transcriptome analysis. Compared with those in the healthy group, we observed obvious changes in the serum lipid subclass content, chain length and unsaturation in the ESCC patients. Integrated lipidomic and transcriptomic analyses revealed that unsaturated fatty acid biosynthesis, fatty acid metabolism, lipid degradation, cholesterol metabolism and the AMPK signaling pathway were enriched in tumor tissues. In addition, RT–qPCR results demonstrated that genes closely related to these pathways were differentially expressed between the ESCC group and the healthy control group. Considering the key role of AMPK in lipid metabolism, we conducted a targeted lipid metabolomics analysis on AMPK-knockdown esophageal cancer cells by UPLC‒MS/MS. These findings suggested that AMPK might be correlated with lipid metabolism in Kazakh ESCC patients, identifying potential therapeutic targets of AMPK and other lipid metabolism-related markers against the progression of ESCC.
2024-01-17 | GSE253171 | GEO
Project description:Esophageal cancer is one of the leading causes of cancer-related mortality because of poor prognosis. Long noncoding RNAs (lncRNAs) have been gradually demonstrated to play critical roles in cancer development. We identified a novel long noncoding RNA named linc00460 by microarray analysis using esophageal squamous cell carcinoma (ESCC) clinical samples, which has not been studied before. Our research indicated that linc00460 was overexpressed in the majority of tumor tissues and ESCC cell lines. Linc00460 expression was positively correlated with ESCC TNM stage, lymph node metastasis, and predicted poor prognosis. In vitro experiments showed that linc00460 depletion suppressed ESCC cell growth through regulating cell proliferation and cell cycle; in additional, linc00460 depletion accelerated ESCC cell apoptosis. We further revealed that linc00460 overexpression was manipulated by transcriptional co-activator CBP/P300 through histone acetylation. Given the high expression and important biological functions of linc00460, we suggest that linc00460 works as an oncogene and might be a valuable prognostic biomarker for ESCC diagnosis and treatment.
| S-EPMC5964888 | biostudies-literature
Project description:The high recurrence rate and poor survival prospects of esophageal squamous cell carcinoma (ESCC) patients after treatment make the ongoing research on chemoprevention drugs for ESCC particularly important. In helping to solve this problem, we screened a large number of FDA-approved drugs and found that levodopa, a drug used to treat Parkinson’s disease, has an inhibitory effect on the growth of ESCC cells. To elucidate the molecular mechanisms, we applied mass spectrometry to investigate the anti-tumor activity of levodopa on ESCC. The results suggest that levodopa can down-regulate oxidative phosphorylation, non-alcoholic fatty liver disease (NAFLD) and parkinson disease pathways. SDHD, NDUFS4 and MT-CO3, major respiratory compounds in the mitochondria, were involved in these pathways. Down-regulation of these proteins is associated with mitochondrial dysfunction. Western blotting and immunofluorescence results confirmed the authenticity of proteomics data. Cell viability assay revealed that mitochondrial activity had been suppressed after levodopa treatment. Mitochondrial membrane potential reduction was detected by JC-1 and TMRE assays. And transmission electron microscope (TEM) analysis indicated that mitochondrial morphology changed. Taken together, levodopa inhibits the growth of ESCC through restraining the mitochondria.
2021-09-08 | PXD013824 | Pride
Project description:Background: Esophageal squamous cell carcinoma (ESCC) is a common invasive malignancy worldwide with poor clinical outcomes. Increasing amount of long non-coding RNAs (lncRNAs) have been reported to be involved in cancer development. However, lncRNAs that are functional in ESCC and the underlying molecular mechanisms remain largely unknown. Methods: Transcriptomic analysis was performed to identify dysregulated lncRNAs in ESCC tissue samples. The high expression of LINC00680 in ESCC was validated by RT-qPCR, and the oncogenic functions of LINC00680 was investigated by cell proliferation, colony formation, migration and invasion assays in ESCC cells in vitro and xenografts derived from ESCC cells in mice. RNA-seq, competitive endogenous RNA (ceRNA) network analysis, and luciferase reporter assays were carried out to identify LINC00680 target genes and the microRNAs (miRNAs) bound to LINC00680. Antisense oligonucleotides (ASOs) were used for in vivo treatment. Results: Transcriptome profiling revealed that a large number of lncRNAs was dysregulated in ESCC tissues. Notably, LINC00680 was highly expressed, and upregulation of LINC00680 was associated with large tumor size, advanced tumor stage, and poor prognosis. Functionally, knockdown of LINC00680 restrained ESCC cell proliferation, colony formation, migration, and invasion in vitro and inhibited tumor growth in vivo. Mechanistically, LINC00680 was found to act as a ceRNA by sponging miR-423-5p to regulate PAK6 (p21-activated kinase 6) expression in ESCC cells. The cell viability and motility inhibition induced by LINC00680 knockdown was significantly reversed upon PAK6 restoration and miR-423-5p inhibition. Furthermore, ASO targeting LINC00680 substantially suppressed ESCC both in vitro and in vivo. Conclusions: An oncogenic lncRNA, LINC00680, was identified in ESCC, which functions as a ceRNA by sponging miR-423-5p to promote PAK6 expression and ESCC. LINC00680/miR-423-5p/PAK6 axis may serve as promising diagnostic and prognostic biomarkers and therapeutic targets for ESCC.
2024-10-10 | GSE185617 | GEO
Project description:Esophageal squamous cell carcinoma (ESCC) is a heterogeneous cancer associated with high mortality rate. In India, it is the 6th most common cause of cancer-related mortality. In this study, we employed high-resolution mass spectrometry-based quantitative proteomics to characterize differential protein expression pattern associated with ESCC. We identified several differentially expressed proteins including PDPN, TOP2A, POSTN and MMP2 that were overexpressed in ESCC. In addition, we identified downregulation of esophagus tissue-enriched proteins such as SLURP1, PADI1, CSTA and small proline-rich proteins like SPRR3, SPRR2A, SPRR1A and CSTA, KRT4, KRT13 involved in squamous cell differentiation. We identified several overexpressed proteins belonging to 3q24-29 chromosomal region, corroborating CNV alterations in this region reported by several published studies. For example, we identified overexpression of SOX2, TP63, IGF2BP2 and RNF13 that are encoded by 3q26 region. Functional enrichment analysis revealed proteins involved in cell cycle pathways, DNA replication, spliceosome, and DNA repair pathways. We identified overexpression of multiple proteins that play a major role in alleviating ER stress. SYVN1/SEL1L complex forms the ER quality control machinery clearing misfolded proteins from ER. SYVN1 is an E3 ubiquitin ligase that ubiquitinates ER-resident proteins. There are also other non-canonical substrates of SYVN1 which are known to play a crucial role in tumor progression. Therefore, SYVN1 is a potential therapeutic target in ESCC.
2023-10-24 | PXD036238 | Pride
Project description:Twelve clinical samples from human esophageal squamous cell carcinoma (ESCC) (seven tumors and five non-tumors) were sequenced using Illumina high-throughput sequencing and the RNA-Seq profiling was investigated with 1730 genes significantly differentially expressed. The gene Rab25 was found to be down-regulated in tumors (p-value < 1E-20) and identified as a novel candidate tumor suppressor gene. The down-regulation of Rab25 was examined in a large cohort of ESCC and non-tumor cases by qPCR and immunohistochemistry analyses. Aberrant methylation in the promoter region of Rab25 was studied by demethylation treatment with 5-aza-dC and bisulfite genomic sequencing (BGS). In order to assess the effect of Rab25 on tumor growth and angiogenesis, in vitro and in vivo functional studies in ESCC cell lines using lentiviral-based overexpression or knockdown models were also performed. 7 tumor and 5 normal samples
2012-12-05 | E-GEOD-32424 | biostudies-arrayexpress
Project description:Our aim is to identify frequent genomic aberrations both in ESCC and esophageal dysplasia, and to discover important copy number-driving genes and microRNAs in ESCC. We carried out array-based comparative genomic hybridization (array CGH) on 59 ESCC resection samples and 16 dysplasia biopsy samples. Expression of genes at 11q13.3 was analyzed by real-time PCR and immunohistochemistry (IHC). Integrated analysis was performed to identify genes or microRNAs with copy number-expression correlations. Two group experiment, esophageal dysplasia vs. esophageal squamous cell carcinoma. Biological replicates: 16 dysplasias vs. 59 carcinomas
2013-04-29 | E-GEOD-46452 | biostudies-arrayexpress
Project description:We used microarrays to determine global gene expression in primary tumor tissues (ESCC) and matched normal tissues (adjacent normal esophageal mucosa) Paired primary ESCC tumor and normal tissues were compared (n=5).
2009-09-01 | E-GEOD-17351 | biostudies-arrayexpress
Project description:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC. We performed a bead array analysis of more than 800 cancer-related genes in a series of 10 ESCC samples, 10 matched surrounding tissues, and 4 esophageal mucosa from healthy individuals. Pyrosequencing was used for validation of DNA methylation changes in up to 106 patients and 27 controls.
2011-11-23 | E-GEOD-26784 | biostudies-arrayexpress
Project description:Preoperative chemoradiotherapy (CRT) followed by surgery has been proved to improve esophageal squamous cell carcinoma (ESCC) patientsM-bM-^@M-^Y survival in comparison with surgery alone. However, the outcomes of CRT are heterogeneous, and no clinical or pathological method could predict CRT response. We aim to identify mRNA markers for ESCC CRT-response prediction through gene expression analyses. Gene expression analyses were performed on pretreatment cancer biopsies from 28 ESCCs who received neoadjuvant CRT and surgery and 10 normal esophageal epithelia using Affymetrix U133 Plus 2.0 arrays.
2014-08-01 | E-GEOD-45670 | biostudies-arrayexpress