Protein Tyrosine Phosphatase 4A3 (PTP4A3) as a Prognostic Biomarker and Pharmacological Target in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) represents a critical focus for biomarker research, given its high mortality, rapid progression, substantial treatment resistance, and marked genetic heterogeneity. The present study identifies PTP4A3 as a relevant molecular determinant in the disease, linking its overexpression to adverse clinical outcomes, genomic instability, activation of oncogenic signaling pathways, and the expansion of poorly differentiated myeloid populations. The integration of in silico analyses with in vitro functional assays demonstrated that pharmacological inhibition of PTP4A3 significantly compromises leukemic cell viability and clonogenic potential, while promoting apoptotic signaling and reducing ERK1/2 phosphorylation in a time-dependent manner. The inhibitor JMS-053 showed consistent antileukemic activity across multiple AML cell models and displayed synergistic effects when combined with cytarabine, a cornerstone of current curative regimens. Collectively, these findings support the role of PTP4A3 as both a prognostic biomarker and a promising therapeutic target in AML, providing a rationale for further investigation of PTP4A3-targeted strategies in preclinical and clinical settings.