HIVEP3 as a potential prognostic factor promotes the development of acute myeloid leukemia

Acute myeloid leukemia (AML) is a common malignancy worldwide. Human immune deficiency virus type 1 enhancer-binding protein 3 (HIVEP3) was verified to play a vital role in types of cancers. However, the functional role of HIVEP3 in AML was rarely reported. In this study, CCK-8, colony formation assay, flow cytometry, and Trans-well chamber experiments were applied for detecting cell proliferation, apoptosis, and invasion in AML cells. The expression of proteins related to TGF-beta/Smad signaling pathway was determined by western blot. Our data showed that the expression level of HIVEP3 was closely related to the risk classification and prognosis of AML patients. Moreover, HIVEP3 was highly expressed in AML patients and cells. Knockdown of HIVEP3 significantly repressed cell proliferation invasion, and enhanced cell apoptosis in HL-60 and THP-1 cells. In addition, HIVEP3 donwreglation could inhibit the TGF-beta/Smad signaling pathway. TGF-beta overexpression could reverse the inhibition effects of HIVEP3 knockdown on AML development and the TGF-beta/Smad signaling pathway. These findings indicated that HIVEP3 contributed to the progression of AML via regulating the TGF-beta/Smad signaling pathway and had a prognostic value for AML.

Automated summary

This study revealed that HIVEP3 plays a crucial role in the progression of AML by regulating the TGF-beta/Smad signaling pathway and has prognostic value for AML.