ArticleNeoplasia (New York, N.Y.)2018
FUS-CHOP Promotes Invasion in Myxoid Liposarcoma through a SRC/FAK/RHO/ROCK-Dependent Pathway.
Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Biomolecular condensates as dynamic regulators of musculoskeletal homeostasis, disease, and therapeutic challenges.Bone research · 2026Review
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- Strictosamide and mitraphylline inhibit cancer cell motility by suppressing epithelial-mesenchymal transition via integrin α4-mediated signaling.Scientific reports · 2025Article
- Challenges and hope: latest research trends in the clinical treatment and prognosis of liposarcoma.Frontiers in pharmacology · 2025Review
- GPX1 expression promotes stemness and aggressiveness in myxoid liposarcomas.International journal of biological sciences · 2025Article
- FUS::DDIT3 Fusion Protein in the Development of Myxoid Liposarcoma and Possible Implications for Therapy.Biomolecules · 2024Review
- Targeting liposarcoma: unveiling molecular pathways and therapeutic opportunities.Frontiers in oncology · 2024Review
- Addressing Doxorubicin Resistance in Bone Sarcomas Using Novel Drug-Resistant Models.International journal of molecular sciences · 2022Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Functional and clinical characteristics of focal adhesion kinases in cancer progression.Frontiers in cell and developmental biology · 2022Review
- The impact of fusion genes on cancer stem cells and drug resistance.Molecular and cellular biochemistry · 2021Review
- Mithramycin delivery systems to develop effective therapies in sarcomas.Journal of nanobiotechnology · 2021Article
- Cancer Stem Cells as a Source of Drug Resistance in Bone Sarcomas.Journal of clinical medicine · 2021Review
- Nano-Encapsulation of Mithramycin in Transfersomes and Polymeric Micelles for the Treatment of Sarcomas.Journal of clinical medicine · 2021Article
- Osteosarcoma tissue-engineered model challenges oxidative stress therapy revealing promoted cancer stem cell properties.Free radical biology & medicine · 2021Article
- GARP promotes the proliferation and therapeutic resistance of bone sarcoma cancer cells through the activation of TGF-β.Cell death & disease · 2020Article
- LINC00205 promotes malignancy in lung cancer by recruiting FUS and stabilizing CSDE1.Bioscience reports · 2020Article
- Modeling neoplastic disease with spheroids and organoids.Journal of hematology & oncology · 2020Review
- Article
- Mechanism of lung adenocarcinoma spine metastasis induced by CXCL17.Cellular oncology (Dordrecht, Netherlands) · 2020Article
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulated SRC/FAK signaling leads to enhanced migration and invasion in many types of tumors. In myxoid and round cell liposarcoma (MRCLS), an adipocytic tumor characterized by the expression of the fusion oncogene FUS-CHOP, SRC have been found as one of the most activated kinases. Here we used a cell-of-origin model of MRCLS and an MRCLS cell line to thoroughly characterize the mechanisms of cell invasion induced by FUS-CHOP using in vitro (3D spheroid invasion assays) and in vivo (chicken chorioallantoic membrane model) approaches. FUS-CHOP expression activated SRC-FAK signaling and increased the invasive ability of MRCLS cells. In addition, FAK expression was found to significantly correlate with tumor aggressiveness in sarcoma patient samples. The involvement of SRC/FAK activation in FUS-CHOP-mediated invasion was further confirmed using the SRC inhibitor dasatinib, the specific FAK inhibitor PF-573228, and FAK siRNA. Notably, dasatinib and PF573228 could also efficiently block the invasion of cancer stem cell subpopulations. Downstream of SRC/FAK signaling, we found that FUS-CHOP expression increases the levels of the RHO/ROCK downstream effector phospho-MLC2 (T18/S19) and that this activation was prevented by dasatinib or PF573228. Moreover, the ROCK inhibitor RKI-1447 was able to completely abolish invasion in FUS-CHOP-expressing cells. These data uncover the involvement of SRC/FAK/RHO/ROCK signaling axis in FUS-CHOP-mediated invasion, thus providing a rationale for testing inhibitors of this pathway as potential novel antimetastatic agents for MRCLS treatment.
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