Regulatory mechanism of tumor cell proliferation by pluripotency-associated transcriptional repressor NACC1

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Elevated expression of NACC1 associates with tumor recurrence and growth of breast, ovarian and cervical cancers. To clarify the molecular mechanism of tumor growth acceleration by NACC1 overexpression in human malignancies, we determined whether NACC1 regulates beta-catenin/TCF pathway in breast cancer cell lines. In parallel, proteomic analysis of NACC1 interacting proteins was carried out. We identified NACC2, ZKSCAN1 and PLK1 as novel NACC1-intracting proteins. NACC1-PLK1 interaction was elevated in cells synchronized at metaphase compared to asynchronous cells. PLK1 expression and NACC1-PLK1 colocalization was observed specifically in metaphase, whereas NACC1 expression was observed in any cell cycle stages. In addition, NACC1 phosphorylation by PLK1 was elevated by metaphase synchronization.