Recently, emerging evidence has demonstrated that
metastasis-associated
lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNAs (lncRNAs), contributes to the initiation and development of
tumors, including
osteosarcoma (OS). Multiple studies have suggested an oncogenic role of MALAT1 and high-mobility group
protein B1 (
HMGB1) in OS
tumorigenesis and
metastasis, but the effects and mechanisms are not unanimous. Here, we showed that MALAT1 and
HMGB1 were significantly increased in human OS cell lines and knockdown of MALAT1 reduced
HMGB1 expression. By using online tools, we screen out 2 candidate
miRNAs, miR-142-3p and miR-129-5p which may be associated with both MALAT1 and
HMGB1.
Luciferase reporter assay revealed a direct interaction between the 2
miRNAs and MALAT1, respectively, via a putative binding site within MALAT1. Meanwhile, both the 2
miRNAs could bind to
HMGB1 3'-untranslated region (3'-UTR) and regulate
HMGB1 expression. Moreover, knockdown of MALAT1 decreased
HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on
HMGB1 expression, OS cell growth and the promotion of apoptosis. In OS tissues, the expression of MALAT1 and
HMGB1 was upregulated while the expression of miR-142-3p and miR-129-5p was downregulated. Together, our results support a MALAT1/miR-142-3p/miR-129-5p/
HMGB1 axis in OS cell proliferation and
tumor progression. MALAT1 promoted OS cell growth through inhibition of miR-142-3p or miR-129-5p and by targeting
HMGB1.