ArticleStem cells (Dayton, Ohio)2011
Krüppel-like family of transcription factor 9, a differentiation-associated transcription factor, suppresses Notch1 signaling and inhibits glioblastoma-initiating stem cells.
Article in Stem cells (Dayton, Ohio), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 104 citations in OpenAlex.
- INO80 regulates promoter-associated R-loops to coordinate transcription and maintain genome stability in embryonic stem cells.Biological research · 2026Article
- Kruppel-like factor 9 may regulate the inflammatory injury of chondrocytes by affecting NF-κB signaling.Journal of orthopaedic surgery and research · 2025Article
- Nuclear hormone receptors control fundamental processes of human fetal neurodevelopment: Basis for endocrine disruption assessment.Environment international · 2025Article
- KLF9 in cancer: a potential prognostic marker and therapeutic target.Frontiers in oncology · 2025Review
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- Cross talk of tumor protein D52 (TPD52) with KLF9, PKCε, and MicroRNA 223 in ovarian cancer.Journal of ovarian research · 2023Article
- Krüppel-like factor 10 modulates stem cell phenotypes of pancreatic adenocarcinoma by transcriptionally regulating notch receptors.Journal of biomedical science · 2023Article
- Overexpression of Krüppel-Like Factor 9 Enhances the Antitumor Properties of Paclitaxel in Malignant Melanoma-Derived Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Environmental endocrine disruptors and amphibian immunity: A bridge between the thyroid hormone axis and T cell development.Developmental and comparative immunology · 2023Article
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
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- Transcriptome Changes in Glioma Cells Cultivated under Conditions of Neurosphere Formation.Cells · 2022Article
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- KLF9 suppresses cell growth and induces apoptosis via the AR pathway in androgen-dependent prostate cancer cells.Biochemistry and biophysics reports · 2021Article
- Loss of Krüppel-like factor 9 facilitates stemness in ovarian cancer ascites-derived multicellular spheroids via Notch1/slug signaling.Cancer science · 2021Article
- RHOX10 drives mouse spermatogonial stem cell establishment through a transcription factor signaling cascade.Cell reports · 2021Article
- EGFR Activates a TAZ-Driven Oncogenic Program in Glioblastoma.Cancer research · 2021Article
- ISG15 is downregulated by KLF12 and implicated in maintenance of cancer stem cell-like features in cisplatin-resistant ovarian cancer.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Tumor-initiating stem cells (alternatively called cancer stem cells, CSCs) are a subpopulation of tumor cells that plays unique roles in tumor propagation, therapeutic resistance, and tumor recurrence. It is becoming increasingly important to understand the molecular signaling that regulates the self-renewal and differentiation of CSCs. Transcription factors are critical for the regulation of normal and neopolastic stem cells. Here, we examined the expression and function of the Krüppel-like family of transcription factors (KLFs) in human glioblastoma (GBM)-derived neurosphere lines and low-passage primary GBM-derived neurospheres that are enriched for tumor-initiating stem cells. We identify KLF9 as a relatively unique differentiation-induced transcription factor in GBM-derived neurospheres. KLF9 is shown to induce neurosphere cell differentiation, inhibit neurosphere formation, and inhibit neurosphere-derived xenograft growth in vivo. We also show that KLF9 regulates GBM neurosphere cells by binding to the Notch1 promoter and suppressing Notch1 expression and downstream signaling. Our results show for the first time that KLF9 has differentiating and tumor-suppressing functions in tumor-initiating stem cells.
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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.