ArticleFrontiers in cell and developmental biology2021
Retinoic Acid Inhibits Tumor-Associated Mesenchymal Stromal Cell Transformation in Melanoma.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Alisol A 23,24-diacetate improves LPS-induced acute lung injury through the IL-17A/NF-κB signaling pathway.Chinese medicine · 2026Article
- The Spatiotemporal Heterogeneity of Tumor-Associated Stromal Cells: Reprogramming Plasticity to Unlock Precision Cancer Immunotherapy.Cancer communications (London, England) · 2026Review
- The protective role of dietary nutrients in mitigating asthma risks induced by indoor air pollutants: a comparative toxicogenomics perspective.Scientific reports · 2025Article
- Glioblastoma-Associated Mesenchymal Stem/Stromal Cells and Cancer-Associated Fibroblasts: Partners in Crime?International journal of molecular sciences · 2024Review
- The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023Review
- Development and validation of a glioma-associated mesenchymal stem cell-related gene prognostic index for predicting prognosis and guiding individualized therapy in glioma.Stem cell research & therapy · 2023Article
- Targeting the tumor stroma for cancer therapy.Molecular cancer · 2022Review
- Regulation and Function of CCL2 and N-Myc in Retinoic Acid-treated Neuroblastoma Cells.Cancer genomics & proteomicsArticle
- Role of cancer-associated mesenchymal stem cells in the tumor microenvironment: A review.Tzu chi medical journalReview
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
Bone marrow mesenchymal stem/stromal cells (BMSCs) can be transformed into tumor-associated MSCs (TA-MSCs) within the tumor microenvironment to facilitate tumor progression. However, the underline mechanism and potential therapeutic strategy remain unclear. Here, we explored that interleukin 17 (IL-17) cooperating with IFNγ transforms BMSCs into TA-MSCs, which promotes tumor progression by recruiting macrophages/monocytes and myeloid-derived suppressor cells (MDSCs) in murine melanoma. IL-17 and IFNγ transformed TA-MSCs have high expression levels of myelocyte-recruiting chemokines (CCL2, CCL5, CCL7, and CCL20) mediated by activated NF-κB signaling pathway. Furthermore, retinoic acid inhibits NF-κB signaling, decreases chemokine expression, and suppresses the tumor-promoting function of transformed TA-MSCs by prohibiting the recruitment of macrophages/monocytes and MDSCs in the tumor microenvironment. Overall, our findings demonstrate that IL-17 collaborating with IFNγ to induce TA-MSC transformation, which can be targeted by RA for melanoma treatment.
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Registered trials
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