ArticleCancer research2014
TLR9 is critical for glioma stem cell maintenance and targeting.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
- TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Multimodal glioma immunotherapy combining TLR9-targeted STAT3 antisense oligodeoxynucleotides with PD1 immune checkpoint blockade.Neuro-oncology · 2025Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Navigating the Molecular Signaling: Deciphering Cancer Stem Cell Self-Renewal Pathways.International journal of molecular and cellular medicine · 2025Review
- Local CpG-Molecular therapy. Nucleic acids · 2024Article
- Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024Review
- Review
- Investigation of L-carnitine effects on CD44Regenerative therapy · 2023Article
- Review
- Mitophagy bridges DNA sensing with metabolic adaption to expand lung cancer stem-like cells.EMBO reports · 2023Article
- TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.Cellular & molecular biology letters · 2023Review
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- TLR9 and Glioma: Friends or Foes?Cells · 2022Review
- Molecular Pathways and Genomic Landscape of Glioblastoma Stem Cells: Opportunities for Targeted Therapy.Cancers · 2022Review
- Glioma-targeted delivery of exosome-encapsulated antisense oligonucleotides using neural stem cells.Molecular therapy. Nucleic acids · 2022Article
- Toll-like receptors and toll-like receptor-targeted immunotherapy against glioma.Journal of hematology & oncology · 2021Review
- Review
- Toll-Like Receptor 9-Mediated Neuronal Innate Immune Reaction Is Associated with Initiating a Pro-Regenerative State in Neurons of the Dorsal Root Ganglia Non-Associated with Sciatic Nerve Lesion.International journal of molecular sciences · 2021Article
- Differences and similarities between cancer and somatic stem cells: therapeutic implications.Stem cell research & therapy · 2020Review
- Adenovirus infection promotes the formation of glioma stem cells from glioblastoma cells through the TLR9/NEAT1/STAT3 pathway.Cell communication and signaling : CCS · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Understanding supports for cancer stem-like cells in malignant glioma may suggest therapeutic strategies for their elimination. Here, we show that the Toll-like receptor TLR9 is elevated in glioma stem-like cells (GSC) in which it contributes to glioma growth. TLR9 overexpression is regulated by STAT3, which is required for GSC maintenance. Stimulation of TLR9 with a CpG ligand (CpG ODN) promoted GSC growth, whereas silencing TLR9 expression abrogated GSC development. CpG-ODN treatment induced Frizzled4-dependent activation of JAK2, thereby activating STAT3. Targeted delivery of siRNA into GSC was achieved via TLR9 using CpG-siRNA conjugates. Through local or systemic treatment, administration of CpG-Stat3 siRNA to silence STAT3 in vivo reduced GSC along with glioma growth. Our findings identify TLR9 as a functional marker for GSC and a target for the delivery of efficacious therapeutics for glioma treatment. Cancer Res; 74(18); 5218-28. ©2014 AACR.
Indexed as
Identifiers
What OpenQuestion holds
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.