ArticleCancer science2023
Acute myeloid leukemia (AML)-derived mesenchymal stem cells induce chemoresistance and epithelial-mesenchymal transition-like program in AML through IL-6/JAK2/STAT3 signaling.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Recent trends in research on the role of cholesterol in leukemia: a bibliometric and visualization study.Frontiers in immunology · 2025Pooled it
- Discovery of BEND4 as a novel single-gene prognostic marker and therapeutic target for adverse AML.NPJ precision oncology · 2026Article
- Defining alteration in bone marrow mesenchymal stem cells (MSC) from acute myeloid leukemia and exploring cultured MSC-conditioned media as a novel anti-leukemia therapy agent.Cancer immunology, immunotherapy : CII · 2026Article
- Acute myeloid leukemia (AML)-derived bone mesenchymal stem cell exosomal METTL14 promotes AML cell growth and glycolysis by HOXA3/WNT7B axis.Cell biology and toxicology · 2026Article
- Integrative analysis of proteomics and metabolomics reveals amino acid metabolism disorder in adriamycin-resistant acute myeloid leukemia cells.Scientific reports · 2026Article
- The Spatiotemporal Heterogeneity of Tumor-Associated Stromal Cells: Reprogramming Plasticity to Unlock Precision Cancer Immunotherapy.Cancer communications (London, England) · 2026Review
- Construction and Validation of an N7-Methylguanosine-Related Prognostic Model for Acute Myeloid Leukemia.Blood and lymphatic cancer : targets and therapy · 2026Article
- Mesenchymal Stromal Cells: Bridging the Gaps in Hematologic Disease Therapy.Stem cell reviews and reports · 2026Review
- Exploring the Bone Marrow Microenvironment as a Therapeutic Barrier and Targetable Source of Crosstalk in Acute Myeloid Leukemia.Blood and lymphatic cancer : targets and therapy · 2026Review
- Article
- Integrative multiomics analysis of platelet-related genes unveils molecular subtypes and prognostic signatures in acute myeloid leukemia.NPJ precision oncology · 2025Article
- Integrated metabolomic and transcriptomic analysis identifies adipogenic differentiation of mesenchymal stem cells as a driver of chemoresistance in acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2025Article
- Targeting bone marrow mesenchymal stromal cell-derived IL-6 to overcome acute myeloid leukemia chemoresistance.Blood advances · 2025Observational
- Cellular and molecular features of acute myeloid leukemia investigation based on single-cell RNA sequencing.Cancer cell international · 2025Article
- TKT regulates the pentose phosphate pathway via RBKS to promote epithelial-mesenchymal transition during AML progression.Journal of bioenergetics and biomembranes · 2025Article
- Role of interleukin-6 in resistance to tumor therapy.Discover oncology · 2025Review
- Article
- HDAC3-YY1-RAB5A axis remodels AML-supportive niche by modulating mitochondrial homeostasis in bone marrow stromal cells.Cell death & disease · 2025Article
- Mesenchymal stem cells in the bone marrow microenvironment: a double-edged sword for AML.Journal of cancer research and clinical oncology · 2025Review
- Exosome-mediated ferroptosis in the tumor microenvironment: from molecular mechanisms to clinical application.Cell death discovery · 2025Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) has a high rate of treatment failure due to increased prevalence of therapy resistance. Mesenchymal stem cells (MSCs) in the leukemia microenvironment contribute to chemoresistance in AML, but the specific mechanism remains unclear. The critical role of the epithelial-mesenchymal transition (EMT)-like profile in AML chemoresistance has been gradually recognized. However, there is no research to suggest that the AML-derived bone marrow mesenchymal stem cells (AML-MSCs) induce the EMT program in AML thus far. We isolated AML-MSCs and cocultured them with AML cells. We found that AML-MSCs induced a significant mesenchymal-like morphology in drug-resistant AML cells, but it was scarce in parental AML cells. The AML-MSCs promoted growth of AML cells in the presence or absence of chemotherapeutics in vitro and in vivo. Acute myeloid leukemia MSCs also induced EMT marker expression in AML cells, especially in chemoresistant AML cells. Mechanistically, AML-MSCs secreted abundant interleukin-6 (IL-6) and upregulated IL-6 expression in AML cells. Acute myeloid leukemia cells upregulated IL-6 expression in AML-MSCs in turn. Meanwhile, AML-MSCs activated the JAK2/STAT3 pathway in AML cells. Two JAK/STAT pathway inhibitors counteracted the AML-MSCs induced morphology change and EMT marker expression in AML cells. In conclusion, AML-MSCs not only promote the emergence of chemoresistance but also enhance it once AML acquires chemoresistance. AML-MSCs induce EMT-like features in AML cells; this phenotypic change could be related to chemoresistance progression. AML-MSCs induce the EMT-like program in AML cells through IL-6/JAK2/STAT3 signaling, which provides a therapeutic target to reverse chemoresistance in AML.
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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.