ArticleDiscover oncology2026
Up-regulation of SLC26A3 enhances oxaliplatin sensitivity in colorectal cancer.
Article in Discover oncology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
The role of SLC26A3 in the sensitivity to oxaliplatin, a widely used chemotherapy drug for colorectal cancer (CRC), remains unclear. This study aimed to explore the association between SLC26A3 expression and oxaliplatin sensitivity. Total 240 differentially expressed mRNAs were identified, with 124 downregulated and 116 upregulated in oxaliplatin-resistant CRC. WGCNA identified a module significantly associated with resistance. GO and KEGG analyses revealed enrichment in fatty acid metabolic processes and organic anion transmembrane transporter activity. PCA and feature gene selection identified a 15-gene signature, with SLC26A3 highlighted by machine learning models as a key discriminator of chemosensitivity. Immunohistochemical staining and survival analysis indicated that higher SLC26A3 expression correlated with better survival outcomes. Additionally, a significant negative correlation between SLC26A3 and AKT1 was observed, suggesting that while SLC26A3 may enhance oxaliplatin sensitivity, its effect may be overshadowed by other factors in resistant cells. SLC26A3 may play a crucial role in oxaliplatin sensitivity in CRC. The identified gene signature could potentially serve as a biomarker for predicting chemosensitivity to oxaliplatin.
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