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Background  We previously identified that the CpG island-associated promoter of the novel lincRNA  ZNF300P1  (also known as  LOC134466 ) is frequently hypermethylated and silenced in ovarian cancer tissues. However, the function of  ZNF300P1  was unknown. In this report we demonstrate that  ZNF300P1  is involved in the regulation of key cell cycle and cell motility networks in human ovarian surface epithelial cells, and may play a role in promoting metastasis in ovarian cancer cells.    Methods  We applied methylated DNA immunoprecipitation on whole genome promoter tiling arrays and Sequenom assays to examine methylation status of  ZNF300P1  in multiple ovarian cancer cell lines, as well as in normal ovarian and ovarian tumor tissues. Transcript profiling was used to investigate the effects of  ZNF300P1  suppression in ovarian cancer cells. We utilized siRNA knockdown in normal ovarian surface epithelial cells and performed cellular proliferation, migration and adhesion assays to validate and explore the profiling results.    Results  We demonstrate that  ZNF300P1  is methylated in multiple ovarian cancer cell lines. Loss of  ZNF300P1  results in decreased cell proliferation and colony formation. In addition, knockdown of the  ZNF300P1  transcript results in aberrant and less persistent migration in wound healing assays due to a loss of cellular polarity. Using an  ex vivo  peritoneal adhesion assay, we also reveal a role for  ZNF300P1  in the attachment of ovarian cancer cells to peritoneal membranes, indicating a potential function of  ZNF300P1  expression in metastasis of ovarian cancer cells to sites within the peritoneal cavity.    Conclusion  Our findings further support  ZNF300P1  as frequently methylated in ovarian cancer and reveal a novel function for  ZNF300P1  lincRNA expression in regulating cell polarity, motility, and adhesion and loss of expression may contribute to the metastatic potential of ovarian cancer cells.

ZNF300P1 Encodes a lincRNA that regulates cell polarity and is epigenetically silenced in type II epithelial ovarian cancer