Overexpression of PTPRZ1 Regulates p120/ β -Catenin Phosphorylation to Promote Carcinogenesis of Oral Submucous Fibrosis

Abstract

Background. Oral submucous fibrosis (OSF) is a potentially malignant disease of the oral cavity. New molecular predictors are needed to identify the high risk of malignant transformation in potentially malignant oral lesions. Our purpose is to explore PTPRZ1 and p120/ $\beta$ -catenin pathogenesis in the carcinogenesis of OSF to identify novel drug targets. Methods. The expression of PTPRZ1, p120, and $\beta$ -catenin in clinical tissues was detected. Then, PTPRZ1, p120, $\beta$ -catenin, RhoA, Rac1, CDC42, cyclin D1, and c-myc expressions were detected by qRT-PCR and western blot. CCK-8 was applied to measure hOMF cells viability. Wound healing and transwell assay were applied to measure cell migration and invasion. Western blot and IF detected the distribution of p-p120 and p- $\beta$ -catenin. Tumor formation experiment explored PTPRZ1 effects on OSF. Results. PTPRZ1, p120, and $\beta$ -catenin were abnormally expressed in cancer tissues. PTPRZ1 regulated the phosphorylation of p120/ $\beta$ -catenin. Western blot and IF showed that in the oe-NC group, p-p120 and p- $\beta$ -catenin were expressed in the cell membrane. p-p120 and p- $\beta$ -catenin were expressed in the cytoplasm and nucleus of the oe-PTPRZ1 group. In vitro experimental results revealed overexpression of PTPRZ1 and $\beta$ -catenin, and silencing of p120 promoted cell proliferation, migration, and invasion. The tumor volume and weight in the sh-PTPRZ1 group were significantly reduced. IHC revealed the positive rate of PTPRZ1 was also low. Conclusions. Overexpression of PTPRZ1 regulated the phosphorylation of p120/ $\beta$ -catenin to promote OSF malignancy.