PTPIP51 is overexpressed in prostate carcinoma compared to benign prostate hyperplasia and in glioblastoma WHO grade IV versus WHO grade II astrocytoma, exhibiting a tissue-specific expression profile. This study links the methylation status of PTPIP51 in prostate carcinoma and benign prostate hyperplasia to altered expression profiles, revealing hypomethylation in prostate cancer that is absent in benign hyperplasia. This hypomethylation likely accounts for the higher protein and mRNA levels of PTPIP51 in prostate cancer. The interaction of PTPIP51 with 14-3-3β forms a ternary complex with cRAF (Raf1), stimulating the downstream EGFR/MAPK signaling pathway, which is critical for cell proliferation and migration in carcinoma progression. Co-localization of PTPIP51 with 14-3-3β, Raf-1, and PTP1B was observed in both prostate carcinoma and glioblastoma. PTP1B, which regulates PTPIP51's phosphorylation and interaction with 14-3-3β, suggests a changed interaction profile in tumors. In glioblastoma, overexpression of EGFR and its mutant form EGFRvIII prompted investigation into PTPIP51's regulatory role on the EGFR/MAPK pathway. Notably, inhibition of EGFR by Gefitinib resulted in downregulation of PTPIP51 and 14-3-3β, highlighting PTPIP51's influence on EGFR signaling. These findings provide a foundation for further studies on PTPIP51 regulation in tumors, particularly its functional implications in neuroepithelial tumors and pote
