Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China.
Department of Orthopedics, Guangzhou First People's Hospital, Guangzhou Guangdong 510182, China.
Oxid Med Cell Longev. 2022 Aug 28;2022:5941562. doi: 10.1155/2022/5941562. eCollection 2022.
The aim of this study is to elucidate molecular mechanism by which E1A-like inhibitor of differentiation 3 (EID3) promotes cancer stem cell-like phenotypes in osteosarcoma. Overexpression of EID3 in osteosarcoma cells generated more spherical clones, enhanced the expression of stemness-associated genes, and promoted chemoresistance, invasion, and metastasis. Furthermore, osteosarcoma cells overexpressing EID3 had increased ability to grow in suspension as osteospheres with high expression of Sox2 and stem cell marker CD133. In addition, knockdown of EID3 reduced sphere formation and inhibited osteosarcoma cell migration and invasion. RNA sequencing and bioinformatics analysis revealed that PI3K-Akt signaling pathway and MAPK pathway-related genes were enriched in osteosarcoma cells with high expression of EID3. Taken together, EID3 promotes osteosarcoma, and EID3-PI3K-Akt axis is a potential therapeutic target for osteosarcoma treatment.
本研究旨在阐明 E1A 样分化抑制因子 3（EID3）促进骨肉瘤中癌症干细胞样表型的分子机制。在骨肉瘤细胞中过表达 EID3 会产生更多的球体克隆，增强干细胞相关基因的表达，并促进化疗耐药性、侵袭和转移。此外，过表达 EID3 的骨肉瘤细胞具有更高的悬浮生长能力，形成具有高表达 Sox2 和干细胞标记物 CD133 的骨球体。此外，EID3 的敲低会减少球体的形成，并抑制骨肉瘤细胞的迁移和侵袭。RNA 测序和生物信息学分析表明，在 EID3 高表达的骨肉瘤细胞中，PI3K-Akt 信号通路和 MAPK 通路相关基因富集。总之，EID3 促进骨肉瘤的发生，EID3-PI3K-Akt 轴是骨肉瘤治疗的潜在治疗靶点。
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