ArticleOncotarget2016
Overexpression of KLF4 promotes cell senescence through microRNA-203-survivin-p21 pathway.
Article in Oncotarget, 2016. 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, 34 citations in OpenAlex.
- Article
- KLF4 in Parkinson's Disease: Decoding the Molecular Puzzle of Neuroinflammation, Oxidative Stress, and Emerging Therapies.Current medical science · 2026Review
- Anti-Müllerian hormone induces a reversible quiescence-associated secretory phenotype in preantral follicles†.Biology of reproduction · 2026Article
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Regulatory Role of Zinc in Acute Promyelocytic Leukemia: Cellular and Molecular Aspects with Therapeutic Implications.International journal of molecular sciences · 2025Review
- Article
- Single-cell profiling reveals age-associated immunity in atherosclerosis.Cardiovascular research · 2023Article
- Selective targeting of α7 nicotinic acetylcholine receptor by synthetic peptide mimicking loop I of human SLURP-1 provides efficient and prolonged therapy of epidermoid carcinomaFrontiers in cell and developmental biology · 2023Article
- A RUNX-targeted gene switch-off approach modulates the BIRC5/PIF1-p21 pathway and reduces glioblastoma growth in mice.Communications biology · 2022Article
- Deletion of SA β-Gal+ cells using senolytics improves muscle regeneration in old mice.Aging cell · 2022Article
- KLF4 Affects Acute Renal Allograft Injury via Binding to MicroRNA-155-5p Promoter to Regulate ERRFI1.Disease markers · 2022Article
- CCM2-deficient endothelial cells undergo a ROCK-dependent reprogramming into senescence-associated secretory phenotype.Angiogenesis · 2021Article
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- Kruppel-like factor 4 upregulates matrix metalloproteinase 13 expression in chondrocytes via mRNA stabilization.Cell and tissue research · 2020Article
- Characterization of sexual size dimorphism and sex-biased genes expression profile in the olive flounder.Molecular biology reports · 2020Article
- Mesenchymal stem cells of Systemic Sclerosis patients, derived from different sources, show a profibrotic microRNA profiling.Scientific reports · 2019Article
- miR-7-5p regulates the proliferation and migration of colorectal cancer cells by negatively regulating the expression of Krüppel-like factor 4.Oncology letters · 2019Article
- Long non-coding RNA TUG1-mediated down-regulation of KLF4 contributes to metastasis and the epithelial-to-mesenchymal transition of colorectal cancer by miR-153-1.Cancer management and research · 2019Article
- Identification of key pathways and genes in endometrial cancer using bioinformatics analyses.Oncology letters · 2019Article
- Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Krüppel-like factor 4 (KLF4) is a transcription factor and functions as a tumor suppressor or tumor promoter in different cancer types. KLF4 regulates many gene expression, thus affects the process of cell proliferation, differentiation, and apoptosis. Recently, KLF4 was reported to induce senescence during the generation of induced pluripotent stem (iPS) cells, but the exact mechanism is still unclear. In this study, we constructed two doxycycline-inducing KLF4 cell models, and demonstrated overexpression of KLF4 could promote cell senescence, detected by senescence-associated β-galactosidase activity assay. Then we confirmed that p21, a key effector of senescence, was directly induced by KLF4. KLF4 could also inhibit survivin, which could indirectly induce p21. By miRNA microarray, we found a series of miRNAs regulated by KLF4 and involved in senescence. We demonstrated that KLF4 could upregulate miR-203, and miR-203 contributed to senescence through miR-203-survivin-p21 pathway. Our results suggest that KLF4 could promote cell senescence through a complex network: miR-203, survivin, and p21, which were all regulated by overexpression of KLF4 and contributed to cell senescence.
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Registered trials
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.