Department of General Surgery, Pudong New Area People's Hospital, China; State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Int J Biol Macromol. 2023 Aug 30;247:125794. doi: 10.1016/j.ijbiomac.2023.125794. Epub 2023 Jul 11.
Colorectal cancer (CRC) is in the forefront of malignancies for its high incidence and mortality. 5-Fluorouracil (5-FU) is one of the most widely used effective drugs for the treatment of CRC. However, there is an urgent need in reducing its systemic side effects and chemoresistance, in order to make 5-FU-based chemotherapy more effective in the treatment of CRC. In this study, engineered CRC cells were established to overexpress miR-323a-3p, which was a tumor suppressor that targeted both EGFR and TYMS. Then miR-323a-3p-loaded exosomes (miR-Exo) were obtained with suitable methods of collection and purification. We found that miR-Exo significantly inhibited CRC cell proliferation and induced apoptosis by the way of targeting EGFR directly in the cells, which eventually led to desirable tumor regression in the cell derived xenograft (CDX) and patient derived xenograft (PDX) tumor mice models. Moreover, we discovered that miR-323a-3p released from miR-Exo directly inhibited the upregulation of thymidylate synthase (TYMS) induced by 5-FU-resistence in CRC cells, resulting in the revival of tumor cytotoxicity from 5-FU. MiR-Exo could effectively induce the CRC cell apoptosis by targeting EGFR and TYMS, and enhance the therapeutic effects of 5-FU on CRC. Our work demonstrates the potency of miR-Exo for advanced CRC biotherapy.
结直肠癌(CRC)的发病率和死亡率都很高,因此处于恶性肿瘤的前列。5-氟尿嘧啶(5-FU)是治疗 CRC 最广泛使用的有效药物之一。然而,迫切需要降低其全身副作用和化学耐药性,以使基于 5-FU 的化疗在治疗 CRC 方面更加有效。在这项研究中,构建了过表达 miR-323a-3p 的工程化 CRC 细胞,miR-323a-3p 是一种肿瘤抑制因子,可靶向 EGFR 和 TYMS。然后用合适的收集和纯化方法获得载有 miR-323a-3p 的外泌体(miR-Exo)。我们发现 miR-Exo 通过直接靶向细胞中的 EGFR 显著抑制 CRC 细胞增殖并诱导细胞凋亡,最终导致细胞衍生异种移植(CDX)和患者衍生异种移植(PDX)肿瘤小鼠模型中的肿瘤消退。此外,我们发现 miR-323a-3p 从 miR-Exo 中释放出来,直接抑制了 5-FU 耐药 CRC 细胞中胸苷酸合成酶(TYMS)的上调,从而恢复了 5-FU 的肿瘤细胞毒性。miR-Exo 可以通过靶向 EGFR 和 TYMS 有效诱导 CRC 细胞凋亡,并增强 5-FU 对 CRC 的治疗效果。我们的工作证明了 miR-Exo 在晚期 CRC 生物治疗中的潜力。