目的：目前对于骨肉瘤（一种对青少年和儿童构成严重威胁的骨癌）尚缺乏有效治疗方法。长链非编码RNA的失调与多种癌症的关联已被证实，包括骨肉瘤。LINC00891在子宫内膜癌、肺癌和甲状腺癌中表达异常，可能与癌症的恶性行为调控有关。然而，LINC00891在骨肉瘤进展中的潜在功能和机制尚不清楚。材料和方法：利用定量逆转录-聚合酶链反应分析了骨肉瘤细胞中LINC00891、miR-27a-3p和TET1 mRNA的表达。通过CCK-8实验和Transwell实验，对骨肉瘤细胞的增殖、迁移和侵袭进行研究。利用西方博莱特法分析了十一转位1（TET1）蛋白的表达。通过荧光素酶实验研究了LINC00891与miR-27a-3p之间的相互作用，以及miR-27a-3p与TET1之间的相互作用。结果：LINC00891在所检测的五株骨肉瘤细胞系中表达显著下调，尤其是在143B和SaoS-2细胞中。质粒转染导致LINC00891过表达，显著抑制了骨肉瘤细胞的增殖、迁移和侵袭。双荧光素酶报告实验发现LINC00891可作为miR-27a-3p的海绵，LINC00891过表达显著降低了miR-27a-3p的表达。在LINC00891过表达的骨肉瘤细胞中，miR-27a-3p模拟转染加速了恶性行为。此外，TET1是miR-27a-3p的新靶基因。LINC00891过表达显著抑制了TET1的蛋白表达，而升高了TET1 mRNA和蛋白的表达。miR-27a-3p过表达抑制了骨肉瘤细胞中的TET1 mRNA和蛋白表达。结论：我们的研究证实LINC00891通过miR-27a-3p/TET1轴减弱了骨肉瘤细胞的增殖和转移。本研究明确了骨肉瘤发展的新机制和治疗靶点。

Objective: There is currently no adequate treatment for osteosarcoma, a bone malignancy that poses a serious threat to adolescents and children. The dysregulation of long noncoding RNAs is associated with many cancers, including osteosarcoma. LINC00891 expression is aberrant in endometrial cancer, lung cancer, and thyroid cancer, and likely regulate the malignant behavior of cancer. However, the potential function and mechanisms of LINC00891 in osteosarcoma progression remain unclear. Materials and Methods: LINC00891, miR-27a-3p, and TET1 mRNA expression in osteosarcoma cells were analyzed using quantitative reverse transcription-polymerase chain reaction. CCK-8 and Transwell experiments were performed on osteosarcoma cells to investigate proliferation, migration, and invasion, respectively. Ten-eleven translocation 1 (TET1) protein was analyzed using western blotting. Luciferase experiment was performed to investigate the interactions between LINC00891 with miR-27a-3p, and miR-27a-3p with TET1. Results: LINC00891 expression was dramatically decreased in the five osteosarcoma cell lines examined, particularly in 143B and SaoS-2 cells. LINC00891 overexpression due to plasmid transfection sharply blocked the proliferation, migration, and invasion of osteosarcoma cells. Dual-luciferase reporter experiments found that LINC00891 sponges miR-27a-3p, and LINC00891 overexpression sharply decreases miR-27a-3p expression. Transfection with miR-27a-3p mimic accelerated the malignant behaviors in LINC00891 overexpressed-osteosarcoma cells. Moreover, TET1 was a novel targeted-gene of miR-27a-3p. TET1 protein was significantly impeded, whereas LINC00891 overexpression elevated TET1 mRNA and protein in osteosarcoma cells. MiR-27a-3p overexpression inhibited TET1 mRNA and protein in osteosarcoma cells. Conclusions: Our study verified that LINC00891 attenuates the proliferation and metastasis of osteosarcoma cells via the miR-27a-3p/TET1 axis. This study clarifies a new mechanism and therapeutic target for the development of osteosarcoma.