Knockdown of long non-coding RNA HOXD-AS1 inhibits the progression of osteosarcoma

Abstract Long non-coding RNA HOXD-AS1 (HOXD-AS1) has recently been shown to be involved in the development and progression of multiple cancers. However, the expression, significance, and biological function of HOXD-AS1 in osteosarcoma (OS) remain unknown. Here, we found that the expression level of HOXD-AS1 was significantly upregulated in OS tissues and cells. Furthermore, high expression of HOXD-AS1 was positively associated with the clinical and pathological characteristics of OS, including tumor stage and lymph node metastasis, and negatively correlated with overall survival rate. in vitro assays confirmed that knockdown of HOXD-AS1 suppressed cell proliferation, colony formation, migration, and invasion, and promoted cell cycle arrest at G1 stage and apoptosis in OS cells. in vivo assays confirmed that knockdown of HOXD-AS1 significantly decreased tumor growth in xenograft mice, and decreased tumor size and weight. Importantly, we also showed that knockdown of HOXD-AS1 significantly reduced signal transducer and activator of transcription 3 and its target protein (CyclinD1, Bcl-2, and MMP-2) expression in vitro and in vivo . Moreover, overexpression of STAT3 could reverse the suppression of proliferation ability induced by sh-HOXD-AS1 in U2OS cells. Collectively, our data indicated that HOXD-AS1 might be an oncogenic long non-coding RNA (lncRNA) and might be a potential attractive therapeutic target for OS.