ArticleMolecular cancer2015
Sp1 and c-Myc modulate drug resistance of leukemia stem cells by regulating survivin expression through the ERK-MSK MAPK signaling pathway.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 101 citations in OpenAlex.
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- Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026Review
- Unraveling the molecular landscape of Erdheim-Chester disease: new insights from methylome and transcriptome integration.Leukemia · 2025Article
- Regulatory Role of Zinc in Acute Promyelocytic Leukemia: Cellular and Molecular Aspects with Therapeutic Implications.International journal of molecular sciences · 2025Review
- DCAF13 influences breast cancer chemotherapy resistance through metabolic reprogramming by regulating c-Myc expression.Medical oncology (Northwood, London, England) · 2025Article
- E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance.Cell death discovery · 2025Article
- Single-cell epigenetic and clonal analysis decodes disease progression in pediatric acute myeloid leukemia.Blood · 2025Article
- Extrachromosomal circular DNA and their roles in cancer progression.Genes & diseases · 2025Review
- Aurora B facilitates cholangiocarcinoma progression by stabilizing c-Myc.Animal models and experimental medicine · 2024Article
- Signaling pathways governing the behaviors of leukemia stem cells.Genes & diseases · 2024Review
- Interaction and Collaboration of SP1, HIF-1, and MYC in Regulating the Expression of Cancer-Related Genes to Further Enhance Anticancer Drug Development.Current issues in molecular biology · 2023Review
- Sp1 promotes tumour progression by remodelling the mitochondrial network in cervical cancer.Journal of translational medicine · 2023Article
- MORA and EnsembleTFpredictor: An ensemble approach to reveal functional transcription factor regulatory networks.PloS one · 2023Article
- Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.Advances in cancer research · 2023Review
- Dioscin inhibiting EGFR-mediated Survivin expression promotes apoptosis in oral squamous cell carcinoma cells.Journal of Cancer · 2023Article
- Genetic Predisposition to Hepatocellular Carcinoma.Metabolites · 2022Review
- The Wnt/β-catenin signalling pathway in Haematological Neoplasms.Biomarker research · 2022Review
- Acidifiers Attenuate Diquat-Induced Oxidative Stress and Inflammatory Responses by Regulating NF-κB/MAPK/COX-2 Pathways in IPEC-J2 Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Single-Cell FISH Analysis Reveals Distinct Shifts in PKM Isoform Populations during Drug Resistance Acquisition.Biomolecules · 2022Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myeloid leukemia (AML) is initiated and maintained by a subset of self-renewing leukemia stem cells (LSCs), which contribute to the progression, recurrence and therapeutic resistance of leukemia. However, the mechanisms underlying the maintenance of LSCs drug resistance have not been fully defined. In this study, we attempted to elucidate the mechanisms of LSCs drug resistance.
methodsWe performed reverse phase protein arrays to analyze the expression of anti-apoptotic proteins in the LSC-enriched leukemia cell line KG-1a. Immuno-blotting, cell viability and clinical AML samples were evaluated to verify the micro-assay results. The characteristics and transcriptional regulation of survivin were analyzed with the relative luciferase reporter assay, mutant constructs, chromatin immuno-precipitation (ChIP), quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR), and western blotting. The levels of Sp1, c-Myc, phospho-extracellular signal-regulated kinase (p-ERK), phospho-mitogen and stress-activated protein kinase (p-MSK) were investigated in paired CD34+ and CD34- AML patient samples.
resultsSurvivin was highly over-expressed in CD34 + CD38- KG-1a cells and paired CD34+ AML patients compared with their differentiated counterparts. Functionally, survivin contributes to the drug resistance of LSCs, and Sp1 and c-Myc concurrently regulate levels of survivin transcription. Clinically, Sp1 and c-Myc were significantly up-regulated and positively correlated with survivin in CD34+ AML patients. Moreover, Sp1 and c-Myc were further activated by the ERK/MSK mitogen-activated protein kinase (MAPK) signaling pathway, modulating survivin levels.
conclusionOur findings demonstrated that ERK/MSK/Sp1/c-Myc axis functioned as a critical regulator of survivin expression in LSCs, offering a potential new therapeutic strategy for LSCs therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.