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HIVEP3 as a potential prognostic factor promotes the development of acute myeloid leukemia.
Tang, Yanfei; Xu, Guangtao; Hu, Bo; Zhu, Yuzhang.
Afiliação
  • Tang Y; Department of Pediatrics, The Second Affiliated Hospital of Jiaxing University, Jiaxing, PR China.
  • Xu G; Department of Pathology, Forensci and Pathology Laboratory, Jiaxing University Medical College, Jiaxing, PR China.
  • Hu B; Department of Pathology and Municipal Key-Innovative Discipline of Molecular Diagnostics, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing University, Jiaxing, PR China.
  • Zhu Y; Department of Oncology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, PR China.
Growth Factors ; 41(1): 43-56, 2023 02.
Article em En | MEDLINE | ID: mdl-36571205
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-ß/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-ß/Smad signaling pathway. TGF-ß overexpression could reverse the inhibition effects of HIVEP3 knockdown on AML development and the TGF-ß/Smad signaling pathway. These findings indicated that HIVEP3 contributed to the progression of AML via regulating the TGF-ß/Smad signaling pathway and had a prognostic value for AML.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article