HOTAIR may contribute to the malignant phenotype and chemoresistance through competitive binding with miR-29b and by the indirect regulation of PTEN via SP1, followed by the inhibitory regulation of PTEN on PI3K (Zhang et al., 2022); 4) in osteosarcoma (OS), HOTAIR and STAT3 are significantly increased, while miR-106a-5p is dramatically decreased in cisplatin-resistant (DDP) OS tissues as well as Saos/DDP, MG-63/DDP, and U2OS7DDP cells. This evidence concerns the gene HOTAIR and osteosarcoma.