LINC00673 promotes osteosarcoma progression through the miR-92b-3p/DUSP1 axis

An increase body of research indicates that long non-coding RNAs (lncRNAs) play a critical role in the development of osteosarcoma. This study investigates the function and molecular mechanism of LINC00673 in the progression of osteosarcoma.

Quantitative reverse transcription-PCR (qRT-PCR) was employed to assess the expression levels of LINC00673 in osteosarcoma cells and tissues. Additionally, we evaluated the correlation between LINC00673 expression in osteosarcoma tissues and the clinicopathological characteristics of patients. Various assays, including CCK-8, Colony formation assay, Transwell assay, and nude animal model experiments, were conducted to investigate the biological function of LINC00673 in osteosarcoma both in vivo and vitro. Downstream target genes of LINC00673 were identified through whole transcriptome sequencing and bioinformatics tools, followed by validation using qRT-PCR, western blotting, RNA immunoprecipitation (RIP) assay, dual-luciferase reporter gene assay and rescue experiments.

In our study, we found that LINC00673 is highly expressed in osteosarcoma cells and tissues. The upregulation of LINC00673 was positively correlated with advanced clinical stages and distant metastasis in patients with osteosarcoma. The knockdown of LINC00673 suppressed both cell proliferation and metastasis of osteosarcoma in vivo and vitro. Subsequent mechanistic studies revealed that LINC00673 functions as a competing endogenous RNA (ceRNA). enhancing DUSP1 expression by sponging miR-92b-3p.

LINC00673 functions as an oncogenic lncRNA in osteosarcoma by enhancing the malignant phenotype of osteosarcoma through miR-92b-3p/DUSP1 axis.