Overexpression of PTPN21 promotes proliferation of EGF-stimulated acute lymphoblastic leukemia cells via the MAPK signaling pathways

• Published in: Hematology (Luxembourg) Vol. 29; no. 1; p. 2356292
• Main Authors: Zhu, Ni, Wei, Jieping, Wang, Li-Mengmeng, Huang, He, Xiao, Haowen
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis Group 01.12.2024
• Subjects: Acute lymphoblastic leukemia; Apoptosis - drug effects; Cell Line, Tumor; Cell Proliferation - drug effects; Epidermal Growth Factor - pharmacology; Humans; MAP Kinase Signaling System - drug effects; MAPK signal pathways; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism; Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology; proliferation; Protein Tyrosine Phosphatases, Non-Receptor - genetics; Protein Tyrosine Phosphatases, Non-Receptor - metabolism; PTPN21; Src; MAPK signal pathways; PTPN21; Acute lymphoblastic leukemia; proliferation; Src
• ISSN: 1607-8454; 1607-8454
• DOI: 10.1080/16078454.2024.2356292

This study aims to investigate the role of excessive Protein Tyrosine Phosphatase Non-Receptor Type 21 (PTPN21) in the proliferation of Acute Lymphoblastic Leukemia (ALL) cells with EGF stimulation. PTPN21 was overexpressed in ALL cell lines by lentiviral transfection. Apoptosis was assayed by Annexin V/7-AAD staining. The proliferation and cell cycle of EGF-treated ALL cells were assessed by MTT and Ki-67/7-AAD staining respectively. The phosphorylation of Src tyrosine kinase and mediators of distinct MAPK pathways were assessed by Western blot. Overexpression of PTPN21 had minimal effect on the apoptosis of ALL cells, but significantly promoted the proliferation and cell cycle progression of ALL cells stimulated with EGF. The activity of Src tyrosine kinase and the MAPK pathways was elevated. Inhibition of MAPK pathways by specific inhibitors mitigated this pro-proliferative effect of excessive PTPN21 on EGF-stimulated ALL cells. PTPN21 may facilitate ALL progression by promoting cell proliferation via the Src/MAPK signaling pathways.