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-β/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-β/Smad signaling pathway. TGF-β overexpression could reverse the inhibition effects of HIVEP3 knockdown on AML development and the TGF-β/Smad signaling pathway. These findings indicated that HIVEP3 contributed to the progression of AML via regulating the TGF-β/Smad signaling pathway and had a prognostic value for AML.
Keyphrases
- acute myeloid leukemia
- transforming growth factor
- signaling pathway
- induced apoptosis
- cell cycle arrest
- pi k akt
- epithelial mesenchymal transition
- cell proliferation
- prognostic factors
- allogeneic hematopoietic stem cell transplantation
- binding protein
- endoplasmic reticulum stress
- end stage renal disease
- ejection fraction
- oxidative stress
- flow cytometry
- newly diagnosed
- chronic kidney disease
- poor prognosis
- cell cycle
- transcription factor
- machine learning
- endothelial cells
- cell death
- electronic health record
- risk assessment
- long non coding rna
- high throughput
- cell migration
- deep learning
- big data
- artificial intelligence
- human health
- climate change