GOT2 regulates aspartate levels and viability in acute myeloid leukemia cells

Objective To investigate the function of the glutamic-oxaloacetic transaminase 2(GOT2) gene in acute myeloid leukemia cells. Methods ShRNAs targeting at GOT2 were constructed to suppress GOT2 expression in the THP-1 human monocytic leukemia cell line. GOT2 mRNA level was measured by RT-qPCR, and GOT2 protein expression was measured by Western blot. Intracellular free amino acid level was quantified using colorimetric assays. The impact of GOT2 knockdown in THP-1 cell function was evaluated through cell viability (CCK-8 assay) and apoptosis (flow cytometry). Results After GOT2 knockdown, both GOT2 mRNA and protein were significantly decreased in THP-1 cells(P＜0.05). Compared to the control group, GOT2 knockdown did not affect intracellular glutamate levels(P＞0.05), but led to a marked decrease in aspartate level(P＜0.05). GOT2 knockdown significantly impaired THP-1 cell viability, inhibited cell proliferation(P＜0.05) and promoted apoptosis(P＜0.05). Conclusions Down regulation of GOT2 significantly decreases intracellular aspartate level in acute myeloid leukemia cells, impairs cellular viability and induces apoptosis, which suggests that GOT2 may play a key role in the regulation of amino acid metabolism in acute myeloid leukemia.