Connective tissue growth factor stimulates osteosarcoma cell migration and induces osteosarcoma metastasis by upregulating VCAM-1 expression

Hou, Chun‐Han; Yang, Rong‐Sen; Tsao, Ya-Ting

doi:10.1016/j.bcp.2018.06.015

Cited by 24 publications

(17 citation statements)

References 59 publications

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“…Interestingly, it was suggested, that CTGF stimulates osteosarcoma metastasis by upregulating VCAM-1 expression. Additionally, VCAM-1 may have a role in activation of dormant micro metastasis 9,45,46 . CTGF enhances cell motility in breast cancer through integrinαVβ3-ERK1/2 dependent S100A4 upregulation 47 .…”

Section: Ctgf Differentially Regulates Potential Drivers Of Invasion mentioning

confidence: 99%

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling

Hellinger

Schömel

Buse

et al. 2020

Sci Rep

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An altered consistency of tumor microenvironment facilitates the progression of the tumor towards metastasis. Here we combine data from secretome and proteome analysis using mass spectrometry with microarray data from mesenchymal transformed breast cancer cells (MCF-7-EMT) to elucidate the drivers of epithelial-mesenchymal transition (EMT) and cell invasion. Suppression of connective tissue growth factor (CTGF) reduced invasion in 2D and 3D invasion assays and expression of transforming growth factor-beta-induced protein ig-h3 (TGFBI), Zinc finger E-box-binding homeobox 1 (ZEB1) and lysyl oxidase (LOX), while the adhesion of cell-extracellular matrix (ECM) in mesenchymal transformed breast cancer cells is increased. In contrast, an enhanced expression of CTGF leads to an increased 3D invasion, expression of fibronectin 1 (FN1), secreted protein acidic and cysteine rich (SPARC) and CD44 and a reduced cell ECM adhesion. Gonadotropin-releasing hormone (GnRH) agonist Triptorelin reduces CTGF expression in a Ras homolog family member A (RhoA)-dependent manner. Our results suggest that CTGF drives breast cancer cell invasion in vitro and therefore could be an attractive therapeutic target for drug development to prevent the spread of breast cancer.

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Section: Ctgf Differentially Regulates Potential Drivers Of Invasion mentioning

confidence: 99%

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling

Hellinger

Schömel

Buse

et al. 2020

Sci Rep

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“…Among which, CCN2, an oncogene reported in OS, has been screened out. 13 Therefore, we employed a dual-luciferase reporter gene assay to evaluate whether CCN2 could be targeted by miR-584 in OS cells ( Figure 4A). Then we examined the mRNA expression of CCN2 in 37 OS patients by RT-qPCR.…”

Section: Ccn2 May Interact With Mir-584 In Os Cellsmentioning

confidence: 99%

“…12 Moreover, the activation of nuclear factor-kappa B (NF-κB) was participated in CCN2-modulated metastasis in OS. 13 Besides, classical NF-κB could be repressed by upregulation of the IκBα super suppressor in OS cells. 14 Bioinformatics analysis provided forceful evidences that there were potential binding sites between miR-584 and CCN2.…”

Section: Introductionmentioning

confidence: 99%

<p>MicroRNA-584 Impairs Cellular Proliferation and Sensitizes Osteosarcoma Cells to Cisplatin and Taxanes by Targeting CCN2</p>

Li¹,

Kong²,

Zang³

et al. 2020

CMAR

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Background: Osteosarcoma (OS), an aggressive malignant neoplasm, exhibits osteoblastic differentiation. Cisplatin (DDP) and taxanes are among the most effective drugs for OS patients. Nevertheless, the drug resistance remains a main limitation to efficacious chemotherapy in OS. The current report sets to explore the biological function of microRNA-584 (miR-584) and the potential mechanism underlying OS cells resistance to these two drugs. Materials and Methods: The expression profiles of miR-584 and connective tissue growth factor (CTGF, CCN2) in OS tissue samples and cell lines were tested by means of reverse transcription-quantitative polymerase chain reaction and Western blot. U2OS and MG63 cell lines were delivered with miR-584 mimic alone or plus CCN2 to excavate theirs functions by cell counting kit-8 and EdU, flow cytometric analysis, as well as transwell assay, severally. Western bot analysis was conducted to examine the expression of IκBα, pIκBα, NF-κB and pNF-κB. Dual-luciferase reporter gene assay was carried out to assess the targets of miR-584. Results: The downregulation of miR-584 was identified in OS tissues and cells, which was closely linked to the dismal prognosis of OS patients. Overexpression of miR-584 repressed cell viability, migration as well as invasion, potentiated apoptosis and sensitized OS cells to DDP and taxanes. Mechanism investigation specified a direct targeting relationship between CCN2 and miR-584 in OS. Conclusion: In conclusion, miR-584 has the potency to act as a therapeutic maneuver for OS mainly by inducing the chemosensitivity of OS cells to DDP and taxanes.

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“…VEGF expression has been associated with vessel density and decreased disease-free survival of osteosarcoma patients [78, 79]. CTGF was recently shown to promote angiogenesis, increase MMP-2/3 expression and cell migration in osteosarcoma, whereas knockdown of CTGF reduced lung metastasis in an experimental mouse model [80–82]. Other studies have shown that CTGF can increase drug resistance in osteosarcoma as well as regulate VEGF production from fibroblasts [83, 84].…”

Section: Regulators Of Metastasis In the Mesenchymal Tumor Microenvirmentioning

confidence: 99%

The Tumor Microenvironment of Pediatric Sarcoma: Mesenchymal Mechanisms Regulating Cell Migration and Metastasis

et al. 2019

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Purpose of Review This review presents a selection of regulatory molecules of tumor microenvironmental properties and metastasis. Signaling pathways controlling mesenchymal biology in bone and soft-tissue sarcomas found in children and adolescents are prioritized. Recent Findings The tumor microenvironment of pediatric tumors is still relatively unexplored. Highlighted findings are mainly on deregulated genes associated with cell adhesion, migration, and tumor cell dissemination. How these processes are involved in a mesenchymal phenotype and metastasis is further discussed in relation to the epithelial to mesenchymal transition (EMT) in epithelial tumors. Cell plasticity is emerging as a concept with impact on tumor behavior. Summary Sarcomas belong to a heterogeneous group of tumors where local recurrence and tumor spread pose major challenges despite intense multimodal treatments. Molecular pathways involved in the metastatic process are currently being characterized, and tumor-regulatory properties of structural components, and infiltrating, non-malignant cell types should be further investigated.

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Connective tissue growth factor stimulates osteosarcoma cell migration and induces osteosarcoma metastasis by upregulating VCAM-1 expression

Cited by 24 publications

References 59 publications

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling

<p>MicroRNA-584 Impairs Cellular Proliferation and Sensitizes Osteosarcoma Cells to Cisplatin and Taxanes by Targeting CCN2</p>

The Tumor Microenvironment of Pediatric Sarcoma: Mesenchymal Mechanisms Regulating Cell Migration and Metastasis

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