ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Low SLC8A1 in Colorectal Cancer Dictates Radiotherapy Resistance Through Calcium-Dependent ANXA2
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
BACKGROUND AND
aimsTumors actively remodel the tumor microenvironment (TME) to foster therapy resistance. However, the underlying mechanisms remain poorly defined. This study aims to characterize how colorectal cancer (CRC) cells drive TME remodeling to promote radioresistance.
methodsA radioresistant CRC cell line was established via serial in vivo irradiation. Single-cell RNA sequencing characterized TME alterations. The role of tumor-derived small extracellular vesicles (sEVs) in macrophage polarization was assessed. Proteomic analysis identified ANXA2 as a key sEVs cargo, and calcium-dependent sEV secretion was investigated through SLC8A1 modulation. Clinical relevance analyses were further assessed.
resultsThe radioresistant model exhibited enhanced treatment resistance to irradiation and increased infiltration of M2-like tumor-associated macrophages (TAMs), while TAM depletion restored radiosensitivity. Tumor-derived sEVs promoted M2 polarization by activating STAT6 phosphorylation, with ANXA2 as the key functional cargo. Further analysis revealed that SLC8A1 deficiency increased intracellular Ca
conclusionCRC cells with low SLC8A1 expression remodel the TME to foster radioresistance via calcium-dependent secretion of ANXA2
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