Huang Xin, Zhang Weiyue, Pu Feifei, Zhang Zhicai
Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Genes Dis. 2021 Nov 24;10(2):531-541. doi: 10.1016/j.gendis.2021.11.004. eCollection 2023 Mar.
This study aimed to investigate the role of long non-coding RNA maternally expressed gene 3 (lncRNA MEG3) in chemosensitivity of osteosarcoma (OS), and to reveal the possible underlying mechanisms. In this study, we found that the expression of lncRNA MEG3 was significantly lower in OS tissues and cell lines. Furthermore, lncRNA MEG3 overexpression enhanced chemosensitivity of OS by inhibiting cell proliferation, migration, autophagy, and promoting antitumor immunity. LncRNA MEG3 functioned as miR-21-5 sponge to regulate p53 expression in OS. Mechanically, lncRNA MEG3 promoted OS chemosensitivity by regulating antitumor immunity via miR-21-5p/p53 pathway and autophagy. Collectively, this study provided the evidence that lncRNA MEG3 might be a promising therapeutic target for OS chemoresistance.
本研究旨在探讨长链非编码RNA母系表达基因3（lncRNA MEG3）在骨肉瘤（OS）化疗敏感性中的作用，并揭示其可能的潜在机制。在本研究中，我们发现lncRNA MEG3在OS组织和细胞系中的表达显著降低。此外，lncRNA MEG3过表达通过抑制细胞增殖、迁移、自噬和促进抗肿瘤免疫来增强OS的化疗敏感性。lncRNA MEG3作为miR-21-5的海绵体来调节OS中的p53表达。机制上，lncRNA MEG3通过miR-21-5p/p53途径和自噬调节抗肿瘤免疫，从而促进OS的化疗敏感性。总的来说，本研究提供了证据表明lncRNA MEG3可能是OS化疗耐药的一个有前景的治疗靶点。
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