β-arrestin1Facilitates The Proliferation Of Acute T Cell Lymphoblastic Leukemia Cell By Regulating TAL1Expression

Objective: β-arrestin1served as a nuclear transcriptional regulator,has a pivotal role in hematopoiesis. In our previous study, β-arrestin1wasfounded enriched in pediatric acute lymphoblastic leukemia. However, themechanism that β-arrestin1regulated the progress of acute lymphoblasticleukemia, especially in T cell acute lymphoblastic leukemia (T-ALL) wasunknown.Methods: Lentiviral vector was used to knock-down or overexpressthe genes transcription in T-ALL cell lines. The cell proliferation wasidentified by CCK-8, colony forming assay and EdU flow cytometrystaining. The whole genome expression was tested by Affymetrix U133Plus2.0microarray and chip results were further confirmed by Real-timeRT-PCR and Western blotting.Results: The results of cell proliferation assays demonstrated that theproliferation of T-ALL Jurkat cell was specifically facilitated by β-arrestin1.The results of Affymetrix U133Plus2.0microarray showed that the geneexpression of Jurkat cell was significant different between Jurkat-siβ1and Jurkat-mock, mainly in the cell proliferation genes. Further results fromReal-time RT-PCR and Western blotting showed that the expression ofTAL1was positive regulated by β-arrestin1in T-ALL Jurkat cell. Inaddition, TAL1expression was found critical for maintaining theproliferation of T-ALL Jurkat cell.Conclusion: β-arrestin1can serve as an oncogene in T-ALL cells byregulating the expression of TAL1, critical for the proliferation of T-ALLcells, which provides a new potential drug target for T-ALL therapeuticstrategy.