Direct contact between tumor cells and platelets initiates a FAK-dependent F3/TGF-β positive feedback loop that promotes tumor progression and EMT in osteosarcoma

Shi, Qianyu; Xu, Jiuhui; Chen, Chenglong; Hu, Xueyu; Wang, Boyang; Zeng, Fanwei; Ren, Tingting; Huang, Yi; Guo, Wei; Tang, Xiaodong; Ji, Tao

doi:10.1016/j.canlet.2024.216902

Cited by 4 publications

References 40 publications

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Small but mighty: Platelets as multifunctional architects of tumor metastasis and immune regulation

Tang,

Shi,

Luo

2024

MedComm – Future Medicine

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Platelets play an irreplaceable role in hemostasis and wound healing. However, beyond these classical roles, as the smallest anucleate cells in the blood stream, they are crucial for immune response which have inflammatory functions through specialized receptors and different signaling pathways, influencing both innate and adaptive immune response. Furthermore, many research have proved that platelets significantly contribute to tumor metastasis and are associated with poor prognoses in cancer patients through its coagulability and supporting an immunosuppressive tumor microenvironment. When tumor cells detach from the primary tumor mass and enter the bloodstream, they rapidly initiate the direct activation and adhesion of platelets, forming a protective microenvironment. This environment shields circulating tumor cells (CTCs) from the mechanical shear forces of blood flow and immune surveillance. Here we delve into the interaction between platelets and immunomodulation and explore the multifaceted roles and underlying mechanisms by which platelets influence tumor cell metastasis and tumor growth. Furthermore, we also discussed the diagnostic role of platelets in cancer occurrence and progression, as well as the feasibility and prospects of targeting platelets for antitumor immunotherapy. This review provides a multidimensional perspective and reference for platelet‐related cancer treatment strategies and diagnosis.

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Small but mighty: Platelets as multifunctional architects of tumor metastasis and immune regulation

Tang,

Shi,

Luo

2024

MedComm – Future Medicine

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Analysis of publicly available transcriptomic data to identify key genes and pathways associated with osteosarcoma metastasis

Horak

2024

Preprint

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Osteosarcoma is the most common bone tumor occurring in children and adolescents. The prognosis of osteosarcoma patients with metastasis is rather poor, availability of prognostic molecular markers would thereby help to distinguish patients with a worse prognosis and to choose appropriate treatment. This study aimed to analyze data from publicly available datasets to identify genes and pathways associated with osteosarcoma onset and metastasis. A total of 8 datasets were analyzed (Target-OS, GSE220538, GSE21257, GSE9508, GSE87624, GSE14359, GSE19276, and GSE36001), and common deregulated genes and abundant pathways were searched. Three downregulated genes, TMBIM4, PKIB and IGKC, were common between metastatic and non-metastatic osteosarcoma tumors. Several abundant GO terms and pathways were identified, including Apoptotic Process (GO:0006915), Regulation Of Phosphatidylinositol 3-Kinase Signaling (GO:0014066), Regulation Of Cell Adhesion Molecule Production (GO:0060353), Positive Regulation Of MAP Kinase Activity (GO:0043406), and KEGG pathway Adherens junction. Analysis of metastasis versus primary tumor revealed 231 common deregulated genes, identified hub genes involved in the organization of cell-cell junctions and surfactant metabolism. Significant enrichment was found in tight junctions, actin cytoskeleton, focal adhesion, muscle contraction proteins, NF-κB, PIK3/Akt/mTOR, AMPK, TNF, and MAPK signaling. 335 common deregulated genes were found between tumor and normal bone, network analysis revealed two clusters involved in cell cycle progression and G2/M transition, and immune response regulation. Abundance was found in p53, TNF, MAPK, and JAK-STAT pathways.Taken together, this study consolidated transcriptomic data from 8 publicly available datasets to identify common deregulated genes and pathways in osteosarcoma development and metastasis.

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Hypoxia inhibits newt skeletal muscle dedifferentiation

Vdovin,

Walters,

Troyanovskiy

et al. 2024

Preprint

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Unlike mammals, newts are able to regenerate lost muscle tissue by dedifferentiating postmitotic muscle cells, which re-enter the cell cycle to form myogenic progenitors. This ability is considered central to the process of limb regeneration, yet the mechanisms underlying it remain poorly understood. Here, we leverage high-resolution time course bulk transcriptomics profiling to characterise molecular changes during differentiation and dedifferentiation of newt myotubes. We uncover that myogenesis is accompanied by a metabolic shift from glycolysis to OXPHOS, which is partially reverted upon dedifferentiation. By analysing early events during dedifferentiation, we identify TGFβ and members of the oxygen-responsive HIF family as putative plasticity inducers. We detect a stark, transient upregulation of HIF3A early during dedifferentiation, followed by a gradual downregulation of HIF2A. Finally, we show that hypoxia inhibits myotube cell cycle re-entry. These data provide a valuable resource to identify regulators of cellular plasticity and offer insights into the impact of oxygen signalling in regenerative processes.

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Direct contact between tumor cells and platelets initiates a FAK-dependent F3/TGF-β positive feedback loop that promotes tumor progression and EMT in osteosarcoma

Cited by 4 publications

References 40 publications

Small but mighty: Platelets as multifunctional architects of tumor metastasis and immune regulation

Small but mighty: Platelets as multifunctional architects of tumor metastasis and immune regulation

Analysis of publicly available transcriptomic data to identify key genes and pathways associated with osteosarcoma metastasis

Hypoxia inhibits newt skeletal muscle dedifferentiation

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