ArticleCancer letters2020
Sustained activation of notch signaling maintains tumor-initiating cells in a murine model of liposarcoma.
Article in Cancer letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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
9 citing papers in PubMed, 8 citations in OpenAlex.
- Tumorigenesis of well-differentiated and dedifferentiated liposarcoma: 12q amplicon architecture, oncogenic cargo, and evolutionary progression.Cancer metastasis reviews · 2026Review
- Notch signaling regulates the secretion of pro-metastatic factors in extracellular vesicles in liposarcoma.Cancer letters · 2026Article
- Molecular mechanisms underlying liposarcoma subtype transition and proteasome-associated targeted interventions.Journal of translational medicine · 2026Review
- Mechanistic insights into the lncRNA-Notch signaling axis in tumors.Frontiers in cell and developmental biology · 2026Review
- Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment.International journal of molecular sciences · 2024Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Targeting liposarcoma: unveiling molecular pathways and therapeutic opportunities.Frontiers in oncology · 2024Review
- Notch signaling regulates a metabolic switch through inhibiting PGC-1α and mitochondrial biogenesis in dedifferentiated liposarcoma.Oncogene · 2023Article
- CD105: tumor diagnosis, prognostic marker and future tumor therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cells in a tumor are heterogeneous, often including a small number of tumor-initiating cells (TICs) and the majority of cancerous and non-cancerous cells. We have previously reported that constitutive activation of Notch signaling in adipocytes of mice leads to dedifferentiated liposarcoma (DDLPS), an aggressive liposarcoma (LPS) with no effective treatment. Here, we explored the role of Notch signaling in cellular heterogeneity of LPS. We performed serial transplantations to enrich for TICs, and derived cells exhibiting sustained Notch activation (mLPS1 cells) and cells with normal Notch activity (mLPS2 cells). Both mLPS1 and mLPS2 cells proliferated rapidly, and neither exhibited contact inhibition. However, only the mLPS1 cells exhibited tumorigenicity and gave rise to LPS upon engraftment into mice. The mLPS1 cells also highly expressed markers of cancer stem cells (Cd133), mesenchymal stem cells (Cd73, Cd90, Cd105, Dlk1) and the long non-coding RNA Rian. By contrast, the mLPS2 cells accumulated lipid droplets and expressed mature adipocyte markers when induced to differentiate. Most importantly, CRISPR-mediated disruption of Notch abrogated the tumorigenic properties of mLPS1 cells. These results reveal a key role of Notch signaling in maintaining TICs in LPS.
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Registered trials
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