ArticleCancer immunology, immunotherapy : CII2016
Resistance to cytotoxicity and sustained release of interleukin-6 and interleukin-8 in the presence of decreased interferon-γ after differentiation of glioblastoma by human natural killer cells.
Article in Cancer immunology, immunotherapy : CII, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- The microenvironment of glioblastoma: in pursuit of universal multimodal immunotherapy.Acta neurologica Belgica · 2026Review
- Targeting the COX-2/PGECancer immunology, immunotherapy : CII · 2026Review
- The promise of immunotherapy for central nervous system tumours.Nature reviews. Immunology · 2026Review
- Review
- Supercharged NK cells: a unique population of NK cells capable of differentiating stem cells and lysis of MHC class I high differentiated tumors.Cell death & disease · 2025Article
- A Novel Signature of Disulfidptosis-Related lncRNAs Predicts Prognosis in Glioma: Evidence From Bioinformatic Analysis and Experiments.International journal of genomics · 2025Article
- Review
- Advances in NK cell therapy for brain tumors.NPJ precision oncology · 2023Review
- The Tumor Immune Microenvironment in Primary CNS Neoplasms: A Review of Current Knowledge and Therapeutic Approaches.International journal of molecular sciences · 2023Review
- Infiltrating natural killer cells bind, lyse and increase chemotherapy efficacy in glioblastoma stem-like tumorospheres.Communications biology · 2022Article
- The shifting paradigm of colorectal cancer treatment: a look into emerging cancer stem cell-directed therapeutics to lead the charge toward complete remission.Expert opinion on biological therapy · 2021Review
- Cystatin F acts as a mediator of immune suppression in glioblastoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Review
- Immunotherapy of Glioblastoma: Current Strategies and Challenges in Tumor Model Development.Cells · 2021Review
- Article
- Mechanisms of Resistance to NK Cell Immunotherapy.Cancers · 2020Review
- Natural Killer Cells: Diverse Functions in Tumor Immunity and Defects in Pre-neoplastic and Neoplastic Stages of Tumorigenesis.Molecular therapy oncolytics · 2020Review
- EpCAM-high liver cancer stem cells resist natural killer cell-mediated cytotoxicity by upregulating CEACAM1.Journal for immunotherapy of cancer · 2020Article
- The Role of NK Cells and Innate Lymphoid Cells in Brain Cancer.Frontiers in immunology · 2020Review
- Recent Advances in Immune Cell Therapy for Glioblastoma.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Natural killer (NK) cells are functionally suppressed in the glioblastoma multiforme (GBM) tumor microenvironment. We have recently shown that survival and differentiation of cancer stem-like cells (CSCs)/poorly differentiated tumors are controlled through two distinct phenotypes of cytotoxic and non-cytotoxic/split anergized NK cells, respectively. In this paper, we studied the function of NK cells against brain CSCs/poorly differentiated GBM and their NK cell-differentiated counterparts. Brain CSCs/poorly differentiated GBM, differentiated by split anergized NK supernatants (supernatants from NK cells treated with IL-2 + anti-CD16mAb) expressed higher levels of CD54, B7H1 and MHC-I and were killed less by the NK cells, whereas their CSCs/poorly differentiated counterparts were highly susceptible to NK cell lysis. Resistance to NK cells and differentiation of brain CSCs/poorly differentiated GBM by split anergized NK cells were mediated by interferon (IFN)-γ and tumor necrosis factor (TNF)-α. Brain CSCs/poorly differentiated GBM expressed low levels of TNFRs and IFN-γRs, and when differentiated and cultured with IL-2-treated NK cells, they induced increased secretion of pro-inflammatory cytokine interleukin (IL)-6 and chemokine IL-8 in the presence of decreased IFN-γ secretion. NK-induced differentiation of brain CSCs/poorly differentiated GBM cells was independent of the function of IL-6 and/or IL-8. The inability of NK cells to lyse GBM tumors and the presence of a sustained release of pro-inflammatory cytokines IL-6 and chemokine IL-8 in the presence of a decreased IFN-γ secretion may lead to the inadequacy of NK cells to differentiate GBM CSCs/poorly differentiated tumors, thus failing to control tumor growth.
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Registered trials
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