ArticleCancer research2016
The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- OCT4 modulates Pomc gene transcription by interfering with specific corticotroph transcription factors.Journal of endocrinological investigation · 2026Article
- Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma.Clinical and experimental medicine · 2026Article
- The Histone Modifier KANSL2 Is an Actionable Biomarker in Multiple Myeloma.Molecular cancer therapeutics · 2026Article
- Nucleoli-localized KANSL2 as an epigenetic regulator of ribosome biogenesis in glioblastoma cells.Communications biology · 2026Article
- Postnatal persistence of hippocampal Cajal-Retzius cells has a crucial role in the establishment of the hippocampal circuit.Development (Cambridge, England) · 2024Article
- Transcriptional regulation by the NSL complex enables diversification of IFT functions in ciliated versus nonciliated cells.Science advances · 2023Article
- S-adenosylhomocysteine hydrolase-like protein 1 (AHCYL1) inhibits lung cancer tumorigenesis by regulating cell plasticity.Biology direct · 2023Article
- Proximity labeling reveals a new in vivo network of interactors for the histone demethylase KDM5.Epigenetics & chromatin · 2023Article
- Noxa and Mcl-1 expression influence the sensitivity to BH3-mimetics that target Bcl-xL in patient-derived glioma stem cells.Scientific reports · 2022Article
- Ropivacaine represses the proliferation, invasion, and migration of glioblastoma via modulating the microRNA-21-5p/KAT8 regulatory NSL complex subunit 2 axis.Bioengineered · 2022Article
- SOX transcription factors and glioma stem cells: Choosing between stemness and differentiation.World journal of stem cells · 2021Review
- An Integrative and Modular Framework to Recapitulate Emergent Behavior in Cell Migration.Frontiers in cell and developmental biology · 2020Article
- Extracellular Vesicles Loaded miRNAs as Potential Modulators Shared Between Glioblastoma, and Parkinson's and Alzheimer's Diseases.Frontiers in cellular neuroscience · 2020Review
- The non-specific lethal (NSL) complex at the crossroads of transcriptional control and cellular homeostasis.EMBO reports · 2019Review
- GECKO is a genetic algorithm to classify and explore high throughput sequencing data.Communications biology · 2019Article
- The POU5F1 gene expression in colorectal cancer: a novel prognostic marker.Surgery today · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. Mechanistic investigations showed that KANSL2 regulates cell self-renewal, which correlates with effects on expression of the stemness transcription factor POU5F1. RNAi-mediated silencing of POU5F1 reduced KANSL2 levels, linking these two genes to stemness control in GBM cells. Together, our findings indicate that KANSL2 acts to regulate the stem cell population in GBM, defining it as a candidate GBM biomarker for clinical use. Cancer Res; 76(18); 5383-94. ©2016 AACR.
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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.