ArticleOncogene2017
Interferon γ is a STAT1-dependent direct inducer of BCL6 expression in imatinib-treated chronic myeloid leukemia cells.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Mitochondrial ETF insufficiency drives neoplastic growth by selectively optimizing cancer bioenergetics.eLife · 2026Article
- Low Renalase Levels in Newly Diagnosed CML: Dysregulation Sensitive to Modulation by Tyrosine Kinase Inhibitors.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- B Cell Lymphoma 6 (BCL6): A Conserved Regulator of Immunity and Beyond.International journal of molecular sciences · 2024Review
- Skin mesenchymal niches maintain and protect AML-initiating stem cells.The Journal of experimental medicine · 2023Article
- B-cell Lymphoma 6 (BCL6): From Master Regulator of Humoral Immunity to Oncogenic Driver in Pediatric Cancers.Molecular cancer research : MCR · 2022Review
- BCL6 is regulated by the MAPK/ELK1 axis and promotes KRAS-driven lung cancer.The Journal of clinical investigation · 2022Article
- Article
- Eliminating chronic myeloid leukemia stem cells by IRAK1/4 inhibitors.Nature communications · 2022Article
- IFNγ directly counteracts imatinib-induced apoptosis of primary human CD34+ CML stem/progenitor cells potentially through the upregulation of multiple key survival factors.Oncoimmunology · 2022Article
- Shedding Light on Targeting Chronic Myeloid Leukemia Stem Cells.Journal of clinical medicine · 2021Review
- Statins Enhance the Molecular Response in Chronic Myeloid Leukemia when Combined with Tyrosine Kinase Inhibitors.Cancers · 2021Article
- Combination of tyrosine kinase inhibitors and the MCL1 inhibitor S63845 exerts synergistic antitumorigenic effects on CML cells.Cell death & disease · 2021Article
- Yin and Yang: The dual effects of interferons on hematopoiesis.Experimental hematology · 2021Review
- A Review on the Therapeutic Role of TKIs in Case of CML in Combination With Epigenetic Drugs.Frontiers in genetics · 2021Review
- Inflammatory Cytokines Shape an Altered Immune Response During Myeloid Malignancies.Frontiers in immunology · 2021Review
- Therapeutic melanoma vaccine with cancer stem cell phenotype represses exhaustion and maintains antigen-specific T cell stemness by up-regulating BCL6.Oncoimmunology · 2020Article
- Druggable Biochemical Pathways and Potential Therapeutic Alternatives to Target Leukemic Stem Cells and Eliminate the Residual Disease in Chronic Myeloid Leukemia.International journal of molecular sciences · 2019Review
- Drug-induced chromatin accessibility changes associate with sensitivity to liver tumor promotion.Life science alliance · 2019Article
- Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis.Molecular genetics & genomic medicine · 2019Article
- Infliximab therapy together with tyrosine kinase inhibition targets leukemic stem cells in chronic myeloid leukemia.BMC cancer · 2019Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-cell CLL/lymphoma 6 (BCL6) exerts oncogenic effects in several human hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib mesylate (IM) treatment. As several lines of evidence suggest that interferon γ (IFNγ) production in CML patients might have a central role in the response to tyrosine kinase inhibitor (TKI) therapy, we analyzed if IFNγ modulates BCL6 expression in CML cells. Although separate IFNγ or IM treatment only slightly upregulated BCL6 expression, combined treatment induced remarkable BCL6 upregulation in CML lines and primary human CD34+ CML stem cells. We proved that during combined treatment, inhibition of constitutive signal transducer and activator of transcription (STAT) 5 activation by IM allowed the specific enhancement of the STAT1 dependent, direct upregulation of BCL6 by IFNγ in CML cells. By using colony-forming assay, we found that IFNγ enhanced the ex vivo colony or cluster-forming capacity of human CML stem cells in the absence or presence of IM, respectively. Furthermore, inhibition of the transcriptional repressor function of BCL6 in the presence of IM and IFNγ almost completely blocked the cluster formation of human CML stem cells. On the other hand, by using small interfering RNA knockdown of BCL6, we demonstrated that in an IM-treated CML line the antiapoptotic effect of IFNγ was independent of BCL6 upregulation. We found that IFNγ also upregulated several antiapoptotic members of the BCL2 and BIRC gene families in CML cells, including the long isoform of MCL1, which proved to be essential for the antiapoptotic effect of IFNγ in an IM-treated CML line. Our results suggest that combination of TKIs with BCL6 and MCL1 inhibitors may potentially lead to the complete eradication of CML stem cells.
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