ArticleCancer letters2025
The SOX4-Semaphorin3C axis promotes esophageal adenocarcinoma progression.
Article in Cancer letters, 2025. 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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14 authors.
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Abstract
Esophageal adenocarcinoma (EAC) is an aggressive malignancy with an approximately 700 % increase in incidence in Western countries over the past four decades. However, the molecular mechanism driving cancer progression remains elusive. In this study we have identified that SOX4, a transcription factor, is enriched in EACs. SOX4 knockdown or deletion leads to a significant reduction in tumor growth and metastasis. Through integrating RNA-Seq and ChIP-Seq we identified Semaphorin 3C (SEMA3C) as an important downstream target of SOX4. Consistently, knockdown of SEMA3C reduced the growth of EAC cells in vitro and xenografts, accompanied by attenuated epithelial-mesenchymal transition. Our findings identifiy a molecular mechanism through which SOX4 regulates SEMA3C to promote tumor progression, offering potential translational therapeutic target (s) for EAC.
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