Isn't it ionic: PDE10 and ASIC2 as potential mediators in the inflammatory pathway of ovarian carcinogenesis

Inflammation associated with incessant ovulation plays a major role in the etiology of epithelial ovarian cancer (EOC). Our previous research suggested that treatment with MCI-030, a Cox-independent NSAID derivative, reduced EOC incidence in a hen model by inhibiting phosphodiesterase 10 (PDE10) and β-catenin. The expression of ASIC2, an acid-sensing ion channel, was differentially decreased in MCI-030 treated hens relative to the control. In a mosaic analysis with a double marker (MADM) murine system of a premalignant EOC, a differential increase was noted in ASIC2 in spatially resolved precursor lesions. Therefore, we aimed to investigate the relationship between PDE10 and ASIC2 expression in EOC and its potential downstream targets, including β-catenin.