ArticleCellular oncology (Dordrecht, Netherlands)2026
A CREM-ITGA2B-MAPK axis drives proliferation and invasiveness in gastric cancer: insights from single-cell analysis.
Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGastric cancer (GC) characterized by profound cellular heterogeneity, with the diversity and interactions of cells within the tumor microenvironment (TME) playing critical roles in tumorigenesis, metastasis, and therapeutic response. However, the underlying mechanisms remain poorly understood. We aimed to elucidate the mechanisms of tumor progression and identify potential therapeutic targets by investigating cellular diversity and communication within the malignant epithelia and tumor microenvironment (TME) in GC.
methodsIn-depth single-cell RNA sequencing (scRNA-seq) analyses were performed on 19 fresh samples from 12 GC patients, encompassing primary tumors, lymph nodes, and omental metastases. Subsequent bioinformatics analyses were conducted to characterize cellular heterogeneity, followed by experimental and clinical sample verifications to elucidate the molecular underpinnings of GC progression.
resultsOur study identified the cAMP response element modulator (CREM) as a key molecular driver for GC progression, which significant upregulation in malignant epithelial cells. CREM activation promotes aggressive tumor phenotypes and correlates with poorer patient outcomes by regulating the ITGA2B promoter and MAPK signaling pathway. Furthermore, we uncovered distinct heterogeneity in T cells and cancer-associated fibroblasts (CAFs) within the GC TME, revealing spatial disparities in immune microenvironments and cell-cell communication across tumor locations.
conclusionBy providing a comprehensive single-cell transcriptomic atlas of GC, this study highlights the pivotal role of CREM in GC progression. These findings deepen our understanding of GC pathogenesis and highlighted the key role of CREM in GC progression and advanced our understanding of GC pathogenesis and offer a foundation for developing targeted, personalized therapeutic strategies.
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