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Mass spectrometry-based proteomics to study gastric cancer progression: pathophysiological molecular characterization

ABSTRACT: This study employs a proteomic approach to characterize early pathological stages of GC, including chronic gastritis (CG), intestinal metaplasia and low-grade dysplasia (MI-DBG), and advanced stages such as EGC and GC. Specifically, this research seeks to (i) identify stage-specific proteomic signatures by determining differentially expressed proteins (DEPs) across lesional and non-lesional tissues at different stages of the disease progression, (ii) explore molecular pathways by analyzing disrupted biological processes to understand their role in GC progression; (iii) characterize shared and distinct protein deregulation patterns between early and advanced stages; and (iv) develop a systems biology framework to map protein interactions and identify key molecular regulators driving GC progression. These insights may contribute to a deeper understanding of GC pathogenesis and could potentially serve for early detection strategies and therapeutic interventions.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Joaquin Fernandez-Irigoyen

PROVIDER: PXD064323 | JPOST Repository | Tue Mar 17 00:00:00 GMT 2026

REPOSITORIES: jPOST

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Project description:Mouse models of intestinal crypt cell differentiation and tumorigenesis have been used to characterize the molecular mechanisms underlying both processes. DNA methylation is a key epigenetic mark and plays an important role in cell identity and differentiation programs and cancer. To get insights into the dynamics of cell differentiation and malignant transformation we have compared the DNA methylation profiles along the mouse small intestine crypt and early stages of carcinogenesis. Genome-scale analysis of DNA methylation together with microarray gene expression have been applied to compare intestinal crypt stem cells (EphB2positive), differentiated cells (EphB2negative), ApcMin/+ adenomas and the corresponding non-tumor adjacent tissue, together with small and large intestine samples and the colon cancer cell line CT26. Compared with late stages, small intestine crypt differentiation and early stages of carcinogenesis display few and relatively small changes in DNA methylation. Hypermethylated loci are largely shared by the two processes and affect the proximities of promoter and enhancer regions, with enrichment in genes regulated by PRC2 and associated with the intestinal stem cell signature. The hypermethylation is progressive, with minute levels in differentiated cells, as compared with intestinal stem cells, and reaching full methylation in advanced stages. Hypomethylation shows different signatures in differentiation and cancer and is already present in the non-tumor tissue adjacent to the adenomas in ApcMin/+mice, but at lower levels than advanced cancers. Taking into account the parallelisms between human and mouse intestinal carcinogenesis, this study provides a reference framework to interpret the alterations found in human cancer. We have analyzed ApcMin/+ adenomas and the corresponding non-tumor adjacent tissue, together with small and large intestine samples and the colon cancer cell line CT26. Samples were in triplicates, except for tissue adjacent to adenoma (in duplicates).

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	E1-HUN-15C.raw	Raw
	E1-HUN-17MC.raw	Raw

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Mass spectrometry-based proteomics to study gastric cancer progression: pathophysiological molecular characterization

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