Panoply™ Human PTPN2 Over-expressing Stable Cell Line

Psoriasis is a recurrent and protracted disease that severely impacts the physical and mental health of patients. Therefore, exploring its pathogenesis is crucial for identifying therapeutic targets. Here, researchers used immunohistochemistry to analyze the expression level of protein tyrosine phosphatase non-receptor type 2 (PTPN2) in psoriasis tissues and an imiquimod-induced mouse model of psoriasis. The results showed that PTPN2 expression was significantly downregulated in psoriasis tissues. Subsequently, this study investigated the in vitro anti-psoriatic properties of PTPN2 in an IL-6-induced psoriasis-like cell model, indicating that PTPN2's inhibition of keratinocyte proliferation may be related to increased STAT3 dephosphorylation and autophagy levels. These findings provide new insights into the autophagy mechanism of psoriatic keratinocytes and may have significant implications for developing novel therapeutic strategies to improve inflammatory homeostasis in psoriatic patients.

To further investigate the overexpression of PTPN2 in a psoriasis cell model, researchers established a psoriasis cell model by stimulating HaCaT cells with 15 ng/mL IL-6. RT-qPCR and Western blot analyses confirmed stable overexpression of PTPN2 in HaCaT cells and psoriasis-like HaCaT cells (Figure 1A-C). CCK-8, EdU, and flow cytometry results showed that PTPN2 overexpression inhibited the proliferation of psoriasis-like HaCaT cells and promoted apoptosis (Figure 1D-H). Simultaneously, Western blot analysis and TEM results indicated that PTPN2 overexpression inhibited STAT3 phosphorylation and promoted autophagy and apoptosis in psoriasis-like HaCaT cells (Figure 1I,J). In summary, these results suggest that PTPN2 can inhibit STAT3 phosphorylation, promote autophagy, and suppress the proliferation of psoriasis-like HaCaT cells.

Figure 1. Effect of PTPN2 overexpression on STAT3, HaCaT cell function, and autophagy. (Liu S, et al., 2024)