KIF18B promotes tumor progression in osteosarcoma by activating β-catenin

Abstract

<b>Objective:</b> Osteosarcoma is a common primary highly malignant bone tumor. Kinesin family member 18B (<i>KIF18B</i>) has been identified as a potential oncogene involved in the development and metastasis of several cancer types. While KIF18B overexpression in osteosarcoma tissue is clearly detected, its specific function in the disease process remains to be established. <b>Methods:</b><i>KIF18B</i> expression was assessed in osteosarcoma tissues and cells. We additionally evaluated the effects of KIF18B on proliferation, migration, and invasion of osteosarcoma cells, both <i>in vitro</i> and <i>in vivo</i>. <b>Results:</b> Our results showed overexpression of <i>KIF18B</i> in osteosarcoma tissues and cells. Knockdown of <i>KIF18B</i> induced G1/S phase arrest and significantly inhibited proliferation, migration, and invasion of osteosarcoma cells, both <i>in vitro</i> and <i>in vivo</i>. <i>KIF18B</i> regulated β-catenin expression at the transcriptional level by controlling nuclear aggregation of ATF2 and at the post-transcriptional level by interacting with the adenomatous polyposis coli (<i>APC</i>) tumor suppressor gene in osteosarcoma cells. <b>Conclusions:</b> KIF18B plays a carcinogenic role in osteosarcoma by regulating expression of β-catenin transcriptionally <i>via</i> decreasing nuclear aggregation of ATF2 or post-transcriptionally through interactions with APC. Our collective findings support the potential utility of KIF18B as a novel prognostic biomarker for osteosarcoma.