目前的研究探讨了肿瘤细胞源性外泌体（Exos）如何介导hsa_circ_0001739/lncRNA AC159540.1来操纵结直肠癌肝转移中的microRNA（miR）-218-5p/FTO-N6-甲基腺苷（m6A）/MYC信号轴使用 ENCORI 和 LncBase 数据库将 (CRC).hsa_circ_0001739 和 lncRNA AC159540.1 确定为 miR-218-5p 的上游调节因子。检测了 miR-218-5p、hsa_circ_0001739、lncRNA AC159540.1、FTO 和 MYC 的表达模式，并进行功能丧失和获得分析，以检查它们对 CRC 细胞生物学功能的影响。纯化SW480细胞来源的Exos，随后进行体外研究，揭示hsa_circ_0001739/lncRNA AC159540.miR-218-5p在CRC组织和细胞中下调而hsa_circ_0001739/lncRNA AC159540.1上调的作用。 hsa_circ_0001739/lncRNA AC159540.1的沉默抑制了CRC细胞的恶性表型。 Exos介导的hsa_circ_0001739/lncRNA AC159540.1竞争性抑制miR-218-5p以升高FTO和MYC。 Exos介导的hsa_circ_0001739/lncRNA AC159540.1在CRC中的诱导作用也在体内得到验证。最终，Exos介导的circ_0001739/lncRNA AC159540.1调控网络对于CRC至关重要，为CRC治疗提供了理论基础。© 2023。作者获得 Springer Nature B.V. 的独家许可。

The current study probed into how tumor cell-derived exosomes (Exos) mediated hsa_circ_0001739/lncRNA AC159540.1 to manipulate microRNA (miR)-218-5p/FTO-N6-methyladenosine (m6A)/MYC signal axis in liver metastasis in colorectal cancer (CRC).hsa_circ_0001739 and lncRNA AC159540.1 were identified as the upstream regulator of miR-218-5p using ENCORI and LncBase databases. Expression patterns of miR-218-5p, hsa_circ_0001739, lncRNA AC159540.1, FTO, and MYC were detected, accompanied by loss-and-gain-of function assays to examine their effects on CRC cell biological functions. SW480 cells-derived Exos were purified, followed by in vitro studies to uncover the effect of hsa_circ_0001739/lncRNA AC159540.miR-218-5p was downregulated while hsa_circ_0001739/lncRNA AC159540.1 was upregulated in CRC tissues and cells. Silencing of hsa_circ_0001739/lncRNA AC159540.1 restrained the malignant phenotypes of CRC cells. Exos-mediated hsa_circ_0001739/lncRNA AC159540.1 competitively inhibited miR-218-5p to elevate FTO and MYC. The inducing role of Exos-mediated hsa_circ_0001739/lncRNA AC159540.1 in CRC was also validated in vivo.Conclusively, Exos-mediated circ_0001739/lncRNA AC159540.1 regulatory network is critical for CRC, offering a theoretical basis for CRC treatment.© 2023. The Author(s), under exclusive licence to Springer Nature B.V.