目的 探讨长链非编码RNA UNC5B-AS1是否通过调控微RNA（miR）-373-5p/Bcl-2相互作用蛋白3样蛋白（BNIP3L）轴影响骨肉瘤细胞恶性表型。方法 采用CCK-8、Transwell、Annexin V/PI及JC-1等体外实验检测细胞增殖、迁移、侵袭与凋亡；用Real-time PCR、Western blotting及免疫组织化学检测UNC5B-AS1、miR-373-5p和BNIP3L在骨肉瘤组织/癌旁组织及hFOB1.19、MG-63、143B、U2OS等骨肉瘤细胞系中的表达；双荧光素酶报告实验验证miR-373-5p对BNIP3L的靶向调控；裸鼠成瘤实验进行相应的体内验证。结果 UNC5B-AS1在MG-63、143B中高表达，沉默UNC5B-AS1后miR-373-5p上调。MiR-373-5p过表达抑制细胞的增殖、迁移和侵袭，促进凋亡，并伴线粒体膜电位下降。BNIP3L及微管相关蛋白1轻链3（LC3Ⅱ/LC3Ⅰ）下降，泛素结合蛋白p62（P62）升高，提示线粒体自噬受抑；双荧光素酶实验表明，miR-373-5p可直接靶向抑制BNIP3L。BNIP3L过表达可部分逆转miR-373-5p对增殖与侵袭的抑制。体内实验显示，BNIP3L促进肿瘤生长，而miR-373-5p可部分抵消该效应。结论 UNC5B-AS1通过 miR-373-5p/BNIP3L 轴调控骨肉瘤细胞增殖、迁移、侵袭与凋亡，其机制可能与线粒体自噬抑制相关。

Objective To investigate whether the long non-coding RNA UNC5B-AS1 (UNC5B-AS1) regulates malignant phenotypes of osteosarcoma cells through the microRNA (miR)-373-5p/Bcl-2 interacting protein 3 like protein (BNIP3L) axis. Methods Cell proliferation, migration/invasion, and apoptosis were assessed using CCK-8 assay, transwell assay, annexin V/PI staining, and JC-1 staining. The expression of UNC5B-AS1, miR-373-5p and BNIP3L was examined by Real-time PCR, Western blotting, and immunohistochemiscal staining in osteosarcoma tissue and adjacent non-tumor tissue, as well as in hFOB1.19 cells and osteosarcoma cell lines (MG-63, 143B and U2OS). Dual-luciferase reporter assay was performed to validate the direct targeting of BNIP3L by miR-373-5p. A nude mouse xenograft model was used for in vivo validation. Results UNC5B-AS1 was highly expressed in MG-63 and 143B cells, and its knockdown significantly increased miR-373-5p levels. Overexpression of miR-373-5p inhibited proliferation and migration/invasion and promoted apoptosis, accompanied by a decrease in mitochondrial membrane potential. BNIP3L and the microtubule-associated protein 1A/1B light chain 3（LC3Ⅱ/LC3Ⅰ）ratio were reduced while ubiquitin-binding protein p62 (P62) increased, suggesting suppressed mitophagy. Dual-luciferase assay confirmed that miR-373-5p directly targets and inhibits BNIP3L. BNIP3L overexpression partially rescued the inhibitory effects of miR-373-5p on proliferation and invasion. In vivo, BNIP3L overexpression promoted tumor growth, whereas miR-373-5p partially attenuated this effect. Conclusion UNC5B-AS1 could modulates osteosarcoma cell proliferation, migration/invasion, and apoptosis via the miR-373-5p/BNIP3L signaling axis.