ArticleInternational journal of cancer2019
JAK-STAT signalling controls cancer stem cell properties including chemotherapy resistance in myxoid liposarcoma.
Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 74 citations in OpenAlex.
- Effect of xeroderma pigmentosum group C on the characteristics and regulatory mechanisms of lung cancer stem cells.International journal of oncology · 2026Article
- Molecular mechanisms underlying liposarcoma subtype transition and proteasome-associated targeted interventions.Journal of translational medicine · 2026Review
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs.Bioscience reports · 2026Article
- Mechanical Stimuli-Induced Manipulation of Malignant Behavior in Bioprinted Cancer Microtissues via PI3K/NF-κB Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Natural product derived phytochemicals as modulators of cancer stemness and drug resistance.Frontiers in oncology · 2026Review
- The resilient subset: cancer stem cells at the core of immunotherapy resistance.Immunotherapy advances · 2026Review
- The Immune Landscape of Canine Soft Tissue Sarcomas as a Model for Human Soft Tissue Sarcomas.Cancers · 2025Article
- Investigation and development of natural products that target chemotherapy resistance factors in cancer cells.Journal of natural medicines · 2025Review
- Deep Introspection Regarding Cumulative Prognostic Factors in Liposarcoma and Atypical Lipomatous Tumor.Medicina (Kaunas, Lithuania) · 2025Article
- MSN/STAT3 drives cancer stemness and chemoresistance via IL-6/LPAR1 ligand receptor complex in triple-negative breast cancer.Breast cancer research : BCR · 2025Article
- Establishment of patient-derived 3D in vitro models of sarcomas: literature review and guidelines on behalf of the FORTRESS working group.Neoplasia (New York, N.Y.) · 2025Review
- Intratumoral heterogeneity of cancer driver genomic alterations in myxoid liposarcomas.Cancer · 2025Article
- Deciphering the mechanistic roles of ADARs in cancer pathogenesis, tumor immune evasion, and drug resistance.Frontiers in immunology · 2025Review
- Challenges and hope: latest research trends in the clinical treatment and prognosis of liposarcoma.Frontiers in pharmacology · 2025Review
- FUS::DDIT3 Fusion Protein in the Development of Myxoid Liposarcoma and Possible Implications for Therapy.Biomolecules · 2024Review
- Targeted therapy of cancer stem cells: inhibition of mTOR in pre-clinical and clinical research.Cell death & disease · 2024Review
- Cancer Stem Cells in Oral Squamous Cell Carcinoma: A Narrative Review on Experimental Characteristics and Methodological Challenges.Biomedicines · 2024Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Deciphering the role of FUS::DDIT3 expression and tumor microenvironment in myxoid liposarcoma development.Journal of translational medicine · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myxoid liposarcoma (MLS) shows extensive intratumoural heterogeneity with distinct subpopulations of tumour cells. Despite improved survival of MLS patients, existing therapies have shortcomings as they fail to target all tumour cells. The nature of chemotherapy-resistant cells in MLS remains unknown. Here, we show that MLS cell lines contained subpopulations of cells that can form spheres, efflux Hoechst dye and resist doxorubicin, all properties attributed to cancer stem cells (CSCs). By single-cell gene expression, western blot, phospho-kinase array, immunoprecipitation, immunohistochemistry, flow cytometry and microarray analysis we showed that a subset of MLS cells expressed JAK-STAT genes with active signalling. JAK1/2 inhibition via ruxolitinib decreased, while stimulation with LIF increased, phosphorylation of STAT3 and the number of cells with CSC properties indicating that JAK-STAT signalling controlled the number of cells with CSC features. We also show that phosphorylated STAT3 interacted with the SWI/SNF complex. We conclude that MLS contains JAK-STAT-regulated subpopulations of cells with CSC features. Combined doxorubicin and ruxolitinib treatment targeted both proliferating cells as well as cells with CSC features, providing new means to circumvent chemotherapy resistance in treatment of MLS patients.
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