{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T19:22:11Z","timestamp":1789154531648,"version":"build-2803163510"},"reference-count":99,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,6,5]],"date-time":"2025-06-05T00:00:00Z","timestamp":1749081600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["iMeta"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Early gastric cancer (EGC) represents a critical stage in preventing and controlling the progression from gastritis to advanced gastric cancer (AGC). Therefore, identifying the single\u2010cell characteristics of EGC, particularly the cellular composition of the tumor microenvironment (TME), as well as identifying potential predictive markers and therapeutic targets, could significantly enhance the monitoring of gastric cancer and improve clinical cure rates. We constructed a comprehensive single\u2010cell RNA sequencing atlas for 184,426 high\u2010quality gastric cancer cells from various stages, utilizing clinical biopsies and surgical samples. Our single\u2010cell atlas highlights the cellular and molecular characteristics of EGC. Eight distinct cell lineage states were identified, and it was observed that the number of epithelial cell meta\u2010clusters gradually decreased, while the number of T&amp;NK, B, plasma, fibroblast, myeloid, and endothelial cells increased with disease progression. Certain epithelial subclusters (metaplastic stem\u2010like cells (MSCs), pit mucous\u2010like cells (PMC\u2010like), proliferating cells), T\u2010cell subclusters (T\n                    <jats:sub>reg<\/jats:sub>\n                    ,\n                    <jats:italic>CCR7<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    naive,\n                    <jats:italic>CH25H<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    CD4\n                    <jats:sup>+<\/jats:sup>\n                    , T\n                    <jats:sub>EM<\/jats:sub>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    , and\n                    <jats:italic>GFPT2<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells), and endothelial subclusters (\n                    <jats:italic>IL\u201033<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    Venous\u20101 and\n                    <jats:italic>AMAMTSL2<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    Artery\u20102) were found to be increased in EGC. The Venous\u20101 subcluster was found to express high levels of\n                    <jats:italic>IL\u201033<\/jats:italic>\n                    . Mechanistically, it was revealed that IL\u201033 enhances the survival and angiogenesis of endothelial cells by upregulating the expression of adhesion proteins CD34 and PECAM1. Patient\u2010derived EGC and AGC organoids were subsequently generated, and it was demonstrated that endothelial\u2010derived IL\u201033 promoted the growth of both EGC and AGC organoids\n                    <jats:italic>ex vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Furthermore, IL\u201033 was found to increase the expression of KRT17 in EGC organoids. Notably, we also found that high expression of IL\u201033 was positively correlated with the depth of invasion and malignancy of EGC. This study provides novel insights into the single\u2010cell components involved in EGC and reveals the role of the\n                    <jats:italic>IL\u201033<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    endothelial subcluster in EGC progression.\n                  <\/jats:p>","DOI":"10.1002\/imt2.70050","type":"journal-article","created":{"date-parts":[[2025,6,6]],"date-time":"2025-06-06T00:49:54Z","timestamp":1749170994000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Single\u2010cell sequencing reveals the role of\n                    <i>IL\u201033<\/i>\n                    <sup>+<\/sup>\n                    endothelial subsets in promoting early gastric cancer progression"],"prefix":"10.1002","volume":"4","author":[{"given":"Li","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Gastroenterology the Second Affiliated Hospital of Chongqing Medical 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