骨肉瘤是一种恶性骨肿瘤，易早期转移，主要影响儿童和青少年。细胞迁移诱导蛋白（CEMIP）在多种肿瘤疾病中起着关键作用，包括骨肉瘤。壳聚糖寡糖（COS）是从壳聚糖中分离得到的寡聚体，已发现对多种癌症具有显著的抗肿瘤活性。本研究探讨COS对骨肉瘤中CEMIP表达的影响以及其潜在机制。本研究进行了体外实验以确认COS对人骨肉瘤细胞的抑制活性。结果表明，COS对人骨肉瘤细胞具有抑制作用，并能显著抑制CEMIP在体外的表达。接下来，我们研究了COS对CEMIP表达的抑制作用，并进行了生物信息学分析，探索了COS对调控CEMIP表达的信号通路的潜在抑制机制。生物信息学分析预测PI3K信号通路与CEMIP表达密切相关，COS对CEMIP表达的抑制作用可能与PI3K信号通路调控有关。本研究结果显示，COS处理显著抑制CEMIP表达和PI3K/AKT/mTOR信号通路，这在体内外都有观察到。本研究证明了COS能抑制与骨肉瘤恶性程度密切相关的CEMIP的表达。这种抑制作用可能归功于COS对体内外PI3K/AKT/mTOR信号通路的抑制。© 2023. 作者。

Osteosarcoma is a malignant bone tumor that is prone to metastasize early and primarily affects children and adolescents. Cell migration-inducing protein (CEMIP) plays a crucial role in the progression and malignancy of various tumor diseases, including osteosarcoma. Chitosan oligosaccharide (COS), an oligomer isolated from chitin, has been found to have significant anti-tumor activity in various cancers. This study investigates the effects of COS on CEMIP expression in osteosarcoma and explores the underlying mechanism. In present study, in vitro experiments were conducted to confirm the inhibitory activity of COS on human osteosarcoma cells. Our results demonstrate that COS possesses inhibitory effects against human osteosarcoma cells and significantly suppresses CEMIP expression in vitro. Next, we studied the inhibition of the expression of CEMIP by COS and then performed bioinformatics analysis to explore the potential inhibitory mechanism of COS against signaling pathways involved in regulating CEMIP expression. Bioinformatics analysis predicted a close association between the PI3K signaling pathway and CEMIP expression and that the inhibitory effect of COS on CEMIP expression may be related to PI3K signaling pathway regulation. The results of this study show that COS treatment significantly inhibits CEMIP expression and the PI3K/AKT/mTOR signaling pathway, as observed both in vitro and in vivo. This study demonstrates that COS could inhibit the expression of CEMIP, which is closely related to osteosarcoma malignancy. This inhibitory effect may be attributed to the inhibition of the PI3K/AKT/mTOR signaling pathway in vitro and in vivo.© 2023. The Author(s).