Lactylome analysis of lysine-lactylated substrates in esophageal squamous cell carcinoma
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ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Longqi Chen
PROVIDER: PXD064038 | iProX | Sun May 18 00:00:00 BST 2025
REPOSITORIES: iProX
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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: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:Dysregulation of histone acetylation is widely implicated in tumorigenesis, yet its specific roles in the progression and metastasis of esophageal squamous cell carcinoma (ESCC) remains unclear. We here profiled the genome-wide landscape of H3K9ac for paired adjacent normal (Nor), primary ESCC (EC) and metastatic lymph node (LNC) esophageal tissues from three ESCC patients. By integrating these data with the corresponding H3K27ac profiles, we identified a distinct epigenetic reprogramming specific to H3K9ac in EC and LNC samples compared to Nor samples, which predominantly targeted genes functionally associated with tumorigenesis and metastasis, and contributed to their transcriptomic aberrations. The findings were further verified by a publicy available single cell RNA-seq data and in vitro experiment, highlighting the potential therapeutic avenues for intervening ESCC through epigenetic modulation via H3K9ac.
2023-06-08 | GSE234346 | GEO
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: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: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:Human esophageal cancer is the sixth leading cause of cancer death worldwide. More than 90% of esophageal cancer is esophageal squamous cell carcinoma (ESCC). However, the etiological cause of ESCC remains unclear. By using gene expression microarray analysis, we aimed to find whether fungal infection is involved in ESCC development. We identified a wide spectrum of molecular signatures in a fungal infection and ESCC mouse model, including alterations involved in epigenetic regulation, cell cycle control, cell proliferation and survival signaling, and inflammation, which share many similarities with human ESCC.
2017-04-01 | GSE80005 | GEO
Project description:To investigate the transcriptional characterization of early esophageal squamous cell carcinoma (ESCC), we performed RNA-sequencing of 10 matched pairs of tumor and adjacent normal tissues of early stage of ESCC patients
2023-09-09 | GSE213565 | GEO
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.
2013-04-29 | GSE46452 | GEO
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.
2011-11-23 | GSE26784 | GEO