A NF-ĸB-Activin A signaling axis enhances prostate cancer metastasis

Chen, Lanpeng; Menna, Marta De; Groenewoud, Arwin; Thalmann, George N.; Julio, Marianna Kruithof-de; Snaar-Jagalska, B. Ewa

doi:10.1038/s41388-019-1103-0

Cited by 35 publications

(30 citation statements)

References 54 publications

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“…( 308 ) Moreover, the CHT microenvironment enhanced Activin A expression, which correlates with increased bone metastasis risk in patients, in prostate cancer cells. ( 309 )…”

Section: Larval Models To Study Bone Metastasismentioning

confidence: 99%

Skeletal Biology and Disease Modeling in Zebrafish

Dietrich

Fiedler

Kurzyukova

et al. 2020

Journal of Bone and Mineral Research

104

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Zebrafish are teleosts (bony fish) that share with mammals a common ancestor belonging to the phylum Osteichthyes, from which their endoskeletal systems have been inherited. Indeed, teleosts and mammals have numerous genetically conserved features in terms of skeletal elements, ossification mechanisms, and bone matrix components in common. Yet differences related to bone morphology and function need to be considered when investigating zebrafish in skeletal research. In this review, we focus on zebrafish skeletal architecture with emphasis on the morphology of the vertebral column and associated anatomical structures. We provide an overview of the different ossification types and osseous cells in zebrafish and describe bone matrix composition at the microscopic tissue level with a focus on assessing mineralization. Processes of bone formation also strongly depend on loading in zebrafish, as we elaborate here. Furthermore, we illustrate the high regenerative capacity of zebrafish bones and present some of the technological advantages of using zebrafish as a model. We highlight zebrafish axial and fin skeleton patterning mechanisms, metabolic bone disease such as after immunosuppressive glucocorticoid treatment, as well as osteogenesis imperfecta (OI) and osteopetrosis research in zebrafish. We conclude with a view of why larval zebrafish xenografts are a powerful tool to study bone metastasis. © 2021 American Society for Bone and Mineral Research (ASBMR).

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“…( 308 ) Moreover, the CHT microenvironment enhanced Activin A expression, which correlates with increased bone metastasis risk in patients, in prostate cancer cells. ( 309 )…”

Section: Larval Models To Study Bone Metastasismentioning

confidence: 99%

Skeletal Biology and Disease Modeling in Zebrafish

Dietrich

Fiedler

Kurzyukova

et al. 2020

Journal of Bone and Mineral Research

104

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“…In addition, ZF myeloid cells were shown to guide human cancer cell extravasation and invasion by reorganizing extracellular matrix at the metastatic site [28]. Moreover, human cancer cells can comparably respond to the ZF microenvironment of ZF and mice comparably, inducing an activation of NF-kB-Activin A signaling axis which drives the metastatic CSC-like phenotype of the cancer cells [37]. Taken together, those studies indicated a functional interaction between human cancer cells and zebrafish microenvironment leading to the metastatic phenotype.…”

Section: Discussionmentioning

confidence: 99%

Zebrafish Microenvironment Elevates EMT and CSC-Like Phenotype of Engrafted Prostate Cancer Cells

Chen

Olszewski

Julio

et al. 2020

Cells

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To visually and genetically trace single-cell dynamics of human prostate cancer (PCa) cells at the early stage of metastasis, a zebrafish (ZF) xenograft model was employed. The phenotypes of intravenously transplanted fluorescent cells were monitored by high-resolution, single-cell intravital confocal and light-sheet imaging. Engrafted osteotropic, androgen independent PCa cells were extravasated from caudle vein, invaded the neighboring tissue, proliferated and formed experimental metastases around caudal hematopoietic tissue (CHT) in four days. Gene expression comparison between cells in culture and in CHT revealed that engrafted PCa cells responded to the ZF microenvironment by elevating expression of epithelial–mesenchymal transition (EMT) and stemness markers. Next, metastatic potentials of ALDHhi cancer stem-like cells (CSCs) and ALDHlow non-CSCs were analyzed in ZF. Engraftment of CSCs induced faster metastatic onset, however after six days both cell subpopulations equally responded to the ZF microenvironment, resulting in the same increase of stemness genes expression including Nanog, Oct-4 and Cripto. Knockdown of Cripto significantly reduced the vimentin/E-cadherin ratio in engrafted cells, indicating that Cripto is required for transduction of the microenvironment signals from the ZF niche to increase mesenchymal potential of cells. Targeting of either Cripto or EMT transcriptional factors Snail 1 and Zeb1 significantly suppressed metastatic growth. These data indicated that zebrafish microenvironment governed the CSC/EMT plasticity of human PCa cells promoting metastasis initiation.

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“…The NF-κB signaling pathway serves important roles during cancer progression ( 27 , 28 ). The expression levels of NF-κB (p65), p-NF-κB inhibitor-α (IκBα) and p-NF-κB inhibitor-β (IKKβ) were higher in proliferative hemangioma compared with involutional hemangioma ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Silencing long non‑coding RNA NEAT1 suppresses the tumorigenesis of infantile hemangioma by competitively binding miR‑33a‑5p to stimulate HIF1α/NF‑κB pathway

Shu

Xing

et al. 2020

Mol Med Rep

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infantile hemangioma (iH) is one of the most common vascular tumors that occurs during childhood, but its pathogenesis is currently not completely understood. even though lncrna nuclear paraspeckle assembly transcript 1 (neaT1) plays vital roles in tumorigenesis of malignant tumors, its roles in iH remain unclear. Therefore, we evaluate the function of lncrna neaT1 in iH. reverse transcription-quantitative Pcr indicated that iH tissues exhibited high expression levels of neaT1 and hypoxia-inducible factor 1α (HiF1α), and low expression levels of the microrna (mir)-33a-5p. Small interfering rna-mediated depletion of neaT1 suppressed hemangioma endothelial cell (Hemec) proliferation, migration and invasion. The data suggested that neaT1 positively regulated HiF1α expression by sponging mir-33a-5p in Hemecs. mir-33a-5p overexpression or HiF1α silencing also acted to suppress Hemec proliferation, migration and invasion. Furthermore, the results indicated that the neaT1/mir-33a-5p/HiF1α axis regulated the nF-κB signaling pathway. collectively, the results revealed that depletion of lncrna neaT1 suppressed the tumorigenesis of iH by competitively binding mir-33a-5p and thereby stimulating the HiF1α/nF-κB signaling pathway.

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A NF-ĸB-Activin A signaling axis enhances prostate cancer metastasis

Cited by 35 publications

References 54 publications

Skeletal Biology and Disease Modeling in Zebrafish

Skeletal Biology and Disease Modeling in Zebrafish

Zebrafish Microenvironment Elevates EMT and CSC-Like Phenotype of Engrafted Prostate Cancer Cells

Silencing long non‑coding RNA NEAT1 suppresses the tumorigenesis of infantile hemangioma by competitively binding miR‑33a‑5p to stimulate HIF1α/NF‑κB pathway

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