WISP-3 inhibition of miR-452 promotes VEGF-A expression in chondrosarcoma cells and induces endothelial progenitor cells angiogenesis

Lin, Chen‐Yuan; Tzeng, Huey En; Li, Te Mao; Chen, Hsien Te; Lee, Yi; Yang, Yi; Wang, Shih‐Wei; Yang, Wei; Tang, Chih Hsin

doi:10.18632/oncotarget.17142

Cited by 31 publications

(29 citation statements)

References 43 publications

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“…16 MiR-126 is highly induced by long-term laminar shear stress, which subsequently causes the upregulation or downregulation of genes involved in atherosclerosis. [18][19][20] Our previous results indicated that shear stress induces the expression of miR-34a, which promotes endothelial differentiation of EPCs. [18][19][20] Our previous results indicated that shear stress induces the expression of miR-34a, which promotes endothelial differentiation of EPCs.…”

Section: Introductionmentioning

confidence: 95%

MicroRNA‐129‐1‐3p regulates cyclic stretch–induced endothelial progenitor cell differentiation by targeting Runx2

Wang

Bao

et al. 2018

J of Cellular Biochemistry

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Endothelial progenitor cells (EPCs) are vital to the recovery of endothelial function and maintenance of vascular homeostasis. EPCs mobilize to sites of vessel injury and differentiate into mature endothelial cells (ECs). Locally mobilized EPCs are exposed to cyclic stretch caused by blood flow, which is important for EPC differentiation. MicroRNAs (miRNAs) have emerged as key regulators of several cellular processes. However, the role of miRNAs in cyclic stretch–induced EPC differentiation remains unclear. Here, we investigate the effects of microRNA‐129‐1‐3p (miR‐129‐1‐3p) and its novel target Runt‐related transcription factor 2 (Runx2) on EPC differentiation induced by cyclic stretch. Bone marrow‐derived EPCs were exposed to cyclic stretch with a magnitude of 5% (which mimics physiological mechanical stress) at a constant frequency of 1.25 Hz for 24 hours. The results from a miRNA array revealed that cyclic stretch significantly decreased miR‐129‐1‐3p expression. Furthermore, we found that downregulation of miR‐129‐1‐3p during cyclic stretch–induced EPC differentiation toward ECs. Meanwhile, expression of Runx2, a putative target gene of miR‐129‐1‐3p, was increased as a result of cyclic stretch. A 3′UTR reporter assay validated Runx2 as a direct target of miR‐129‐1‐3p. Furthermore, small interfering RNA (siRNA)‐mediated knockdown of Runx2 inhibited EPC differentiation into ECs and attenuated EPC tube formation via modulation of vascular endothelial growth factor (VEGF) secretion from EPCs in vitro. Our findings demonstrated that cyclic stretch suppresses miR‐129‐1‐3p expression, which in turn activates Runx2 and VEGF to promote endothelial differentiation of EPCs and angiogenesis. Therefore, targeting miR‐129‐1‐3p and Runx2 may be a potential therapeutic strategy for treating vessel injury.

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Section: Introductionmentioning

confidence: 95%

MicroRNA‐129‐1‐3p regulates cyclic stretch–induced endothelial progenitor cell differentiation by targeting Runx2

Wang

Bao

et al. 2018

J of Cellular Biochemistry

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“…41 Highly migratory JJ012(S10) cells were selected in our laboratory, according to our previous methods. 42 , 43 Subpopulations of JJ012 cells were examined by Transwell assay and selected according to their differential invasiveness. After overnight migration, cells that had penetrated through pores and migrated to the underside of filters were trypsinized and harvested for a second round of selection.…”

Section: Methodsmentioning

confidence: 99%

Brain-derived neurotrophic factor promotes VEGF-C-dependent lymphangiogenesis by suppressing miR-624-3p in human chondrosarcoma cells

et al. 2017

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Chondrosarcoma is the second most common primary malignancy of bone, and one of the most difficult bone tumors to diagnose and treat. It is well known that increased levels of vascular endothelial growth factor-C (VEGF-C) promote active tumor lymphangiogenesis and lymphatic tumor spread to regional lymph nodes. Brain-derived neurotrophic factor (BDNF) is known to promote metastasis in human chondrosarcoma cells. Knowing more about the mechanism of BDNF in VEGF-C expression and lymphangiogenesis in human chondrosarcoma would improve our understanding as how to prevent chondrosarcoma angiogenesis and metastasis, which currently lacks effective adjuvant treatment. Here, we found that BDNF expression was at least 2.5-fold higher in the highly migratory JJ012(S10) cell line as compared with the primordial cell line (JJ012). In addition, VEGF-C expression and secretion was markedly increased in JJ012(S10) cells. Conditioned medium from JJ012(S10) cells significantly promoted migration and tube formation of human lymphatic endothelial cells (LECs), whereas knockdown of BDNF attenuated LEC migration and tube formation by suppressing VEGF-C production in JJ012(S10) cells. Mechanistic investigations indicated that BDNF facilitated VEGF-C-dependent lymphangiogenesis through the MEK/ERK/mTOR signaling pathway. We also showed that microRNA (miR)-624-3p expression was negatively regulated by BDNF via the MEK/ERK/mTOR cascade. Importantly, BDNF knockdown profoundly inhibited tumor-associated lymphangiogenesis in vivo. Further analyses identified that BDNF promoted tumor lymphangiogenesis by downregulating miR-624-3p in human chondrosarcoma tissues. In conclusion, this study is the first to reveal the mechanism underlying BDNF-induced lymphangiogenesis. We suggest that BDNF may serve as a promising therapeutic target for the restriction of VEGF-C-mediated tumor lymphangiogenesis and lymphatic metastasis.

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“…In chondrosarcoma, VEGF-A expression was found to correlate with adiponectin expression and tumor stage [182]. In this tumor type, the high expression of WNT1-inducible signaling pathway protein-3 (WISP-3) stimulated angiogenesis by downregulating miR-452 that in turn is able to inhibit the expression of VEGF-A [183].…”

Section: Bone Cancermentioning

confidence: 99%

Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models

Ceci

Atzori

Lacal

et al. 2020

IJMS

175

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The vascular endothelial growth factor (VEGF) family members, VEGF-A, placenta growth factor (PlGF), and to a lesser extent VEGF-B, play an essential role in tumor-associated angiogenesis, tissue infiltration, and metastasis formation. Although VEGF-A can activate both VEGFR-1 and VEGFR-2 membrane receptors, PlGF and VEGF-B exclusively interact with VEGFR-1. Differently from VEGFR-2, which is involved both in physiological and pathological angiogenesis, in the adult VEGFR-1 is required only for pathological angiogenesis. Besides this role in tumor endothelium, ligand-mediated stimulation of VEGFR-1 expressed in tumor cells may directly induce cell chemotaxis and extracellular matrix invasion. Furthermore, VEGFR-1 activation in myeloid progenitors and tumor-associated macrophages favors cancer immune escape through the release of immunosuppressive cytokines. These properties have prompted a number of preclinical and clinical studies to analyze VEGFR-1 involvement in the metastatic process. The aim of the present review is to highlight the contribution of VEGFs/VEGFR-1 signaling in the progression of different tumor types and to provide an overview of the therapeutic approaches targeting VEGFR-1 currently under investigation.

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WISP-3 inhibition of miR-452 promotes VEGF-A expression in chondrosarcoma cells and induces endothelial progenitor cells angiogenesis

Cited by 31 publications

References 43 publications

MicroRNA‐129‐1‐3p regulates cyclic stretch–induced endothelial progenitor cell differentiation by targeting Runx2

MicroRNA‐129‐1‐3p regulates cyclic stretch–induced endothelial progenitor cell differentiation by targeting Runx2

Brain-derived neurotrophic factor promotes VEGF-C-dependent lymphangiogenesis by suppressing miR-624-3p in human chondrosarcoma cells

Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models

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