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The transcription factor Ikaros was originally found to function as a keyregulator of lymphocyte differentiation. In this study, we provide the first evidencethat Ikaros is expressed at higher levels in ovarian cancer tissues compared withnormal ovarian tissues and is significantly associated with high FIGO stage andlow differentiation state in ovarian serous adenocarcinoma. To this end, we transfectedIK1 (full length of Ikaros) into the SKOV3 ovarian cancer cell line and examinedcell biological behaviors including proliferation, migration and invasion. Wefound that overexpression of IK1 inhibited cell proliferation by inducing G1 arrest,accompanied by the upregulation of P27 and P21 and downregulation of cyclin D1and D2. On the other hand, IK1 increased the migration and invasion of ovariancancer cells, as assessed by scratch-wound assay, transwell migration assay, andinvasion assay. Overexpression of IK1 significantly increased Slug but not Snail1expression at both mRNA and protein levels. It also downregulated and upregulatedE-cadherin and MMP-2, two target genes of Slug involved in migration, respectively.Furthermore, knocking down Slug abrogated IK1-mediated increase in migration andinvasion. These data suggest that Slug plays an important role in IK1-inducedmigration and invasion. In conclusion, we show for the first time that IK1 playsa dual role in the proliferation, migration and invasion of ovarian cancer cells,providing new insights into their metastasis.

Ikaros inhibits proliferation and, through upregulation of Slug, increases metastatic ability of ovarian serous adenocarcinoma cells