ArticleMolecular oncology2013
KLF4 overexpression and apigenin treatment down regulated anti-apoptotic Bcl-2 proteins and matrix metalloproteinases to control growth of human malignant neuroblastoma SK-N-DZ and IMR-32 cells.
Article in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Krüppel-like factor 4 downregulation during esophageal cancer formation facilitates immune evasion and impairs immunotherapy.Signal transduction and targeted therapy · 2026Article
- Natural Flavonoid Apigenin, an Effective Agent Against Nervous System Cancers.Molecular neurobiology · 2024Review
- Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading.International journal of molecular sciences · 2024Review
- Role of YY1 in the Regulation of Anti-Apoptotic Gene Products in Drug-Resistant Cancer Cells.Cancers · 2023Review
- Stem cell therapy for pulmonary arterial hypertension: An update.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2022Review
- Role of Induced Programmed Cell Death in the Chemopreventive Potential of Apigenin.International journal of molecular sciences · 2022Review
- The deubiquitinase OTUD1 inhibits non-small cell lung cancer progression by deubiquitinating and stabilizing KLF4.Thoracic cancer · 2022Article
- Article
- miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4.Stem cell research & therapy · 2018Article
- The novel KLF4/PLAC8 signaling pathway regulates lung cancer growth.Cell death & disease · 2018Article
- Beneficial Effect of Jojoba Seed Extracts on Hyperglycemia-Induced Oxidative Stress in RINm5f Beta Cells.Nutrients · 2018Article
- Plant flavone apigenin: An emerging anticancer agent.Current pharmacology reports · 2017Article
- MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4.Journal of bone oncology · 2016Article
- Article
- The Transcription Regulator Krüppel-Like Factor 4 and Its Dual Roles of Oncogene in Glioblastoma and Tumor Suppressor in Neuroblastoma.Forum on immunopathological diseases and therapeutics · 2016Article
- MicroRNA-92a Promotes Colorectal Cancer Cell Growth and Migration by Inhibiting KLF4.Oncology research · 2016Article
- Effects of miRNA-145 on airway smooth muscle cells function.Molecular and cellular biochemistry · 2015Article
- Regulation of anti-apoptotic signaling by Kruppel-like factors 4 and 5 mediates lapatinib resistance in breast cancer.Cell death & disease · 2015Article
- EWS Knockdown and Taxifolin Treatment Induced Differentiation and Removed DNA Methylation from p53 Promoter to Promote Expression of Puma and Noxa for Apoptosis in Ewing's Sarcoma.Journal of cancer therapy · 2014Article
- MiR-7 promotes epithelial cell transformation by targeting the tumor suppressor KLF4.PloS one · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroblastoma is a childhood tumor that arises from immature neuroblasts of the sympathetic nervous system. Krüpple-like factor 4 (KLF4) is a transcription factor, the precise function of which in neuroblastoma is unclear. We examined the effects of KLF4 overexpression and apigenin (APG) treatment in human malignant neuroblastoma SK-N-DZ and IMR-32 cell lines. KLF4 overexpression in both SK-N-DZ and IMR-32 cell lines was confirmed by laser scanning immunofluorescent confocal microscopy and Western blotting. We found that 100 nM KLF4 plasmid and 25 μM APG synergistically inhibited the growth of SK-N-DZ and IMR-32 cells. We also found increase in KLF4 expression in response to treatment with various concentrations of APG. Combination of KLF4 plasmid and APG treatment significantly increased the amounts of apoptosis in both cell lines when compared with control vector or single treatment. We also noticed that the combination therapy decreased expression of the anti-apoptotic proteins Bcl-2 and Mcl-1, increased expression of the pro-apoptotic proteins Bax, Noxa, and Puma, upregulated p53, and caused activation of caspase-3 for cleavage of the inhibitor of caspase-activated DNase (ICAD) leading to completion of apoptosis machinery. Further, combination of KLF4 overexpression and APG treatment was highly effective in inhibiting migration of both neuroblastoma cell lines and was associated with down regulation of matrix metalloproteinases (MMPs) such as MMP-2 and MMP-9. Collectively, our results from this investigation strongly suggest that KLF4 functions as a tumor suppressor and potentiates the anti-cancer activities of APG in two different human malignant neuroblastoma cell lines.
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