ArticleFrontiers of medicine2017
Regulatory mechanism and functional analysis of S100A9 in acute promyelocytic leukemia cells.
Article in Frontiers of medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Therapeutic potential of tumor-associated neutrophils: dual role and phenotypic plasticity.Signal transduction and targeted therapy · 2025Review
- S100A8 and S100A9 in Hematologic Malignancies: From Development to Therapy.International journal of molecular sciences · 2023Review
- Intracellular calprotectin (S100A8/A9) facilitates DNA damage responses and promotes apoptosis in head and neck squamous cell carcinoma.Oral oncology · 2023Article
- Bone marrow stroma cells promote induction of a chemoresistant and prognostic unfavorable S100A8/A9high AML cell subset.Blood advances · 2022Article
- Article
- Pathogenic Roles of S100A8 and S100A9 Proteins in Acute Myeloid and Lymphoid Leukemia: Clinical and Therapeutic Impacts.Molecules (Basel, Switzerland) · 2021Review
- S100 Proteins in Acute Myeloid Leukemia.Neoplasia (New York, N.Y.) · 2018Review
- Calprotectin and the Initiation and Progression of Head and Neck Cancer.Journal of dental research · 2018Review
- The role ofCancer management and research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A9, a calcium-binding protein, participates in the inflammatory process and development of various tumors, thus attracting much attention in the field of cancer biology. This study aimed to investigate the regulatory mechanism of S100A9 and its function involvement in APL. We used real-time quantitative PCR to determine whether PML/RARα affects the expression of S100A9 in NB4 and PR9 cells upon ATRA treatment. ChIP-based PCR and dual-luciferase reporter assay system were used to detect how PML/RARα and PU.1 regulate S100A9 promoter activity. CCK-8 assay and flow cytometry were employed to observe the viability and apoptosis of NB4 cells when S100A9 was overexpressed. Results showed that S100A9 was an ATRA-responsive gene, and PML/RARα was necessary for the ATRA-induced expression of S100A9 in APL cells. In addition, PU.1 could bind to the promoter of S100A9, especially when treated with ATRA in NB4 cells, and promote its activity. More importantly, overexpression of S100A9 induced the apoptosis of NB4 cells and inhibited cell growth. Collectively, our data indicated that PML/RARα and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Furthermore, S100A9 promoted apoptosis in APL cells and affected cell growth.
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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.