ArticleTranslational cancer research2025
Upregulation of spondin-2 indicates poorer clinical outcomes and induces radioresistance in gastric cancer.
Article in Translational cancer research, 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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Abstract
Background: Spondin-2 (SPON2) has been reported to be upregulated in various carcinomas, contributing to cancer progression and metastasis. However, its underlying mechanism in gastric cancer (GC) remains poorly understood. This study aimed to explore the relationship between SPON2 expression, prognostic outcomes, and radiotherapy sensitivity in GC. Methods: Public datasets from the cBioPortal website were used to assess SPON2 expression in GC tissues and its clinical significance. The regulatory role of SPON2 in the cell cycle, apoptosis, DNA damage repair (DDR), proliferation, and migration was investigated using the GC cell line HGC-27 under conditions with or without radiation. Results: SPON2 expression in GC tissues was significantly higher than in normal gastric tissues (P<0.001) and was positively correlated with tumor size (P<0.001). Notably, high SPON2 expression predicted poorer overall survival (OS) in patients with GC (P=0.01). Multivariate analysis identified T stage, N stage, age, and SPON2 level as independent prognostic factors for OS. Overexpression of SPON2 in HGC-27 cells significantly enhanced cell proliferation and migration. Additionally, SPON2 overexpression induced radioresistance and reduced radiation-induced G2/M arrest, apoptosis, and DNA damage in HGC-27 cells. Conclusions: Upregulated SPON2 promotes GC cell proliferation and is associated with poorer OS in patients with GC. SPON2 overexpression induces cellular resistance to radiation, decreasing radiation-induced DNA damage and apoptosis. Therefore, SPON2 may serve as a potential predictor of radiotherapy efficacy and poor prognosis in GC.
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