Luo Fangcheng, Ando Kosei, Takemura Yoshinori, Park Tae-Hwi, Yayama Takafumi, Imai Shinji
Department of Orthopedic Surgery, Shiga University of Medical Science, Otsu 520-2192, Shiga, Japan.
Cancers (Basel). 2025 Sep 6;17(17):2922. doi: 10.3390/cancers17172922.
Osteosarcoma is an aggressive bone tumor with a high risk of lung metastasis, which severely affects patient survival. EMT plays a major role in tumor spread, therapy resistance, and cancer stemness. This review explores how EMT contributes to osteosarcoma metastasis and the underlying molecular mechanisms.
We reviewed recent studies on EMT-related signaling pathways, transcription factors, and regulatory RNAs in osteosarcoma. We also examined the role of the tumor microenvironment.
EMT promotes cell detachment, migration, and lung colonization. Key pathways such as TGF-β, MAPK, PI3K/Akt, STAT3, Notch, and Wnt/β-catenin are involved. Non-coding RNAs further regulate EMT by interacting with these pathways. The tumor microenvironment, including hypoxia and immune cells, also supports EMT and metastasis.
EMT is a key driver of metastasis and poor outcomes in osteosarcoma. Targeting EMT and its regulators may help prevent lung spread and improve treatment. Future strategies combining EMT inhibition with existing therapies could be promising for clinical application.
骨肉瘤是一种侵袭性骨肿瘤，具有较高的肺转移风险，严重影响患者生存。上皮-间质转化（EMT）在肿瘤扩散、治疗耐药性和癌症干性中起主要作用。本综述探讨EMT如何促进骨肉瘤转移及其潜在的分子机制。
我们回顾了近期关于骨肉瘤中EMT相关信号通路、转录因子和调控RNA的研究。我们还研究了肿瘤微环境的作用。
EMT促进细胞脱离、迁移和肺定植。涉及TGF-β、MAPK、PI3K/Akt、STAT3、Notch和Wnt/β-连环蛋白等关键通路。非编码RNA通过与这些通路相互作用进一步调节EMT。肿瘤微环境，包括缺氧和免疫细胞，也支持EMT和转移。
EMT是骨肉瘤转移和不良预后的关键驱动因素。靶向EMT及其调节因子可能有助于预防肺转移并改善治疗。未来将EMT抑制与现有疗法相结合的策略在临床应用中可能很有前景。
