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논문 기본 정보

자료유형
학술저널
저자정보
Junfeng Hu (Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College) Zhengyang Pan (Zhejiang Chinese Medical University) Guoxi Xu (Jinjiang Hospital) Yan Zhang (Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College) Meiling Wu (Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College) Jiahui Yu (Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College) Xujun He (Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College) Wei Zhang (Zhejiang Chinese Medical University)
저널정보
대한위암학회 Journal of Gastric Cancer Journal of Gastric Cancer Vol.24 No.3
발행연도
2024.7
수록면
300 - 315 (16page)
DOI
10.5230/jgc.2024.24.e25

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Purpose Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

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