ArticleJournal of experimental & clinical cancer research : CR2018
INPP4B promotes cell survival via SGK3 activation in NPM1-mutated leukemia.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 37 citations in OpenAlex.
- CRIP1 functions as an oncogene in acute myeloid leukemia by modulating glycolytic metabolic reprogramming.Scientific reports · 2026Article
- CRIP1 knockdown enhances glycolytic dependence and increases sensitivity to 2-Deoxy-D-Glucose in acute myeloid leukemia.Molecular biology reports · 2026Article
- Role of INPP4B in the proliferation, migration, invasion, and survival of human endometrial cancer cells.Histology and histopathology · 2024Article
- Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma.Journal of oncology · 2023Article
- Tumour-derived small extracellular vesicles suppress CD8+ T cell immune function by inhibiting SLC6A8-mediated creatine import in NPM1-mutated acute myeloid leukaemia.Journal of extracellular vesicles · 2021Article
- Construction of a prognostic model with histone modification-related genes and identification of potential drugs in pancreatic cancer.Cancer cell international · 2021Article
- Expression and functional characterization of INPP4B in gallbladder cancer patients and gallbladder cancer cells.BMC cancer · 2021Article
- Ese-3 contributes to colon cancer progression by downregulating EHD2 and transactivating INPP4B.American journal of cancer research · 2021Article
- Identification of 6 Hub Proteins and Protein Risk Signature of Colorectal Cancer.BioMed research international · 2020Article
- Retracted Article: LncRNA ZEB2-AS1 regulates the drug resistance of acute myeloid leukemiaRSC advances · 2019Article
- Investigating the duality ofOncotarget · 2019Article
- Article
- INPP4B promotes colorectal cancer cell proliferation by activating mTORC1 signaling and cap-dependent translation.OncoTargets and therapy · 2019Article
- Up-regulation of EMT-related gene VCAN by NPM1 mutant-driven TGF-β/cPML signalling promotes leukemia cell invasion.Journal of Cancer · 2019Article
- Serum- and glucocorticoid-inducible kinase 3 is a potential oncogene in nasopharyngeal carcinoma.Brazilian journal of otorhinolaryngologyArticle
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAcute myeloid leukemia (AML) with mutated nucleophosmin (NPM1) has been recognized as a distinct leukemia entity in the 2016 World Health Organization (WHO) classification. The genetic events underlying oncogenesis in NPM1-mutated AML that is characterized by a normal karyotype remain unclear. Inositol polyphosphate 4-phosphatase type II (INPP4B), a new factor in the phosphoinositide-3 kinase (PI3K) pathway-associated cancers, has been recently found a clinically relevant role in AML. However, little is known about the specific mechanistic function of INPP4B in NPM1-mutated AML.
methodsThe INPP4B expression levels in NPM1-mutated AML primary blasts and AML OCI-AML3 cell lines were determined by qRT-PCR and western blotting. The effect of INPP4B knockdown on OCI-AML3 leukemia cell proliferation was evaluated, using the Cell Counting Kit-8 and colony formation assay. After INPP4B overexpression or knockdown, the activation of serum and glucocorticoid-regulated kinase 3 (SGK3) and AKT was assessed. The effects of PI3K signaling pathway inhibitors on the levels of p-SGK3 in OCI-AML3 cells were tested. The mass of PI (3,4) P
resultsHigh expression of INPP4B was observed in NPM1-mutated AML. Knockdown of INPP4B repressed cell proliferation in OCI-AML3 cells, whereas recovered INPP4B rescued this inhibitory effect in vitro. Mechanically, INPP4B enhanced phosphorylated SGK3 (p-SGK3) status, but did not affect AKT activation. SGK3 was required for INPP4B-induced cell proliferation in OCI-AML3 cells. High levels of INPP4B were at least partially caused by the NPM1 mutant via ERK/Ets-1 signaling. Finally, high expression of INPP4B showed a trend towards lower overall survival and event-free survival in NPM1-mutated AML patients.
conclusionsOur results indicate that INPP4B promotes leukemia cell survival via SGK3 activation, and INPP4B might be a potential target in the treatment of NPM1-mutated AML.
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