ArticleEMBO molecular medicine2023
Downregulation of stromal syntenin sustains AML development.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Syntenin inhibition impairs stroma-tumor communication in multiple myeloma and improves bortezomib treatment efficiency.HemaSphere · 2025Article
- MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding.Expert opinion on therapeutic targets · 2025Review
- Bone marrow mesenchymal stromal cells support translation in refractory acute myeloid leukemia.Cell reports · 2025Article
- Finding potential targets in cell-based immunotherapy for handling the challenges of acute myeloid leukemia.Frontiers in immunology · 2024Review
- Downregulation of stromal syntenin sustains AML development.EMBO molecular medicine · 2023Article
- Broadening the horizon: potential applications of CAR-T cells beyond current indications.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The crosstalk between cancer and stromal cells plays a critical role in tumor progression. Syntenin is a small scaffold protein involved in the regulation of intercellular communication that is emerging as a target for cancer therapy. Here, we show that certain aggressive forms of acute myeloid leukemia (AML) reduce the expression of syntenin in bone marrow stromal cells (BMSC). Stromal syntenin deficiency, in turn, generates a pro-tumoral microenvironment. From serial transplantations in mice and co-culture experiments, we conclude that syntenin-deficient BMSC stimulate AML aggressiveness by promoting AML cell survival and protein synthesis. This pro-tumoral activity is supported by increased expression of endoglin, a classical marker of BMSC, which in trans stimulates AML translational activity. In short, our study reveals a vicious signaling loop potentially at the heart of AML-stroma crosstalk and unsuspected tumor-suppressive effects of syntenin that need to be considered during systemic targeting of syntenin in cancer therapy.
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Registered trials
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.