Xu et al. from Nanjing Medicine University compared γ-catenin mRNA levels in bone marrow mononuclear cells between naïve primary Acute Myeloid Leukemia (AML) patients and healthy donors. The function of γ-catenin in the pathogenesis of AML was also investigated. The findings of this study were published in Onco Targets Ther in June 2016.
The data showed that γ-catenin mRNA expression levels were significantly higher in AML patients than in healthy donors. Furthermore, patients who had achieved Complete Remission (CR) in one to two cycles had significantly lower γ-catenin mRNA expression levels in comparison to refractory patients with slow responses.
Consequently, clarifying the role of γ-catenin in AML could serve to increase the understanding of the pathological mechanism of the disease in addition to aiding the development a potential biomarker for clinical diagnosis and prognosis.
Dysregulation of γ-catenin may function as an oncogenic factor in various malignancies. We investigated γ-catenin expression in acute myeloid leukemia (AML) and explored its role in the pathogenesis of AML. γ-Catenin was significantly overexpressed in AML patients compared to healthy donors.
The γ -catenin expression in AML patients with lower white blood cells (<30×109/L) was significantly higher than those with higher white blood cells (≥30×109/L). The expression levels of γ-catenin in AML patients with mutated CEBPα were significantly higher than those with unmutated CEBPα. AML patients with lower γ-catenin levels were more likely to achieve complete remission compared with patients who have higher γ-catenin levels. In K562 cells, γ-catenin knockdown suppressed cellular proliferation, while the cellular migration was greatly enhanced. Moreover, knocking down of γ-catenin enhanced the cytotoxicity of decitabine in K562 cells. Our investigation has indicated a potential role of γ-catenin in the pathogenesis of AML.