Visfatin Promotes the Metastatic Potential of Chondrosarcoma Cells by Stimulating AP-1-Dependent MMP-2 Production in the MAPK Pathway

Hung, Shih Ya; Lin, Chen‐Yuan; Yu, Chao; Chen, Hsien Te; Lien, Ming Yu; Huang, Yu; Fong, Yi Chin; Liu, Ju-Fang; Wang, Shih‐Wei; Chen, Wei Cheng; Tang, Chih‐Hsin

doi:10.3390/ijms22168642

Cited by 15 publications

(22 citation statements)

References 43 publications

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“…The loss of the tight junction barrier facilitates metastasis, invasion, and motility of tumors (Martin & Jiang 2009). Similarly, visfatin also facilitates the migration of chondrosarcoma cells in mice through the upregulation of MMP-2 expression (Hung et al 2021). The present findings are consistent with the previous observation that visfatin promotes the migration of a colorectal carcinoma cell line by inducing EMT (Yang et al 2016).…”

Section: Discussionsupporting

confidence: 91%

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

et al. 2023

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Visfatin is an adipokine with nicotinamide phosphoribosyltransferase (NAMPT) activity, the concentration of which is higher in ascitic fluid than in serum, and is associated with ovarian cancer peritoneal dissemination. Furthermore, potentially important effects of visfatin on glucose metabolism have been previously reported. However, the mechanism underlying the effects of visfatin on ovarian cancer cell invasion, and whether this involves altered glucose metabolism, has not been elucidated. Here we tested the hypothesis that visfatin, which can reprogram cancer metabolism, promotes invasion by ovarian cancer spheroids. Visfatin increased glucose transporter (GLUT)1 expression and glucose uptake in adult granulosa cell tumor-derived spheroid cells (KGN), and also increased the activities of hexokinase 2 and lactate dehydrogenase. We showed a visfatin-induced increase in glycolysis in KGN cells. Moreover, visfatin increased the potential invasiveness of KGN spheroid cells by upregulating MMP2 (matrix metalloproteinase 2) and downregulating CLDN3 and CLDN4 (claudin 3 and 4) gene expression. Interestingly, an inhibitor of GLUT1 (STF-31) and lactate dehydrogenase (LDHA) abolished the stimulatory effect of visfatin on the potential invasiveness of KGN cells. More importantly, silencing expression of the NAMPT gene in KGN cells demonstrated its important effect on glycolysis and invasiveness in adult granulosa cell tumor cells. In summary, visfatin appears to increase adult granulosa cell tumor invasiveness through effects on glucose metabolism, and to be an important regulator of glucose metabolism in these cells

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Section: Discussionsupporting

confidence: 91%

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

et al. 2023

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“…As previous studies have determined that visfatin promotes chondrosarcoma metastasis [ 9 ], we examined whether visfatin regulates distinct angiogenic factor expression during angiogenesis in chondrosarcoma cells. Our findings revealed higher levels of PDGF-C gene expression than other angiogenic factors, including ANGPD-1 , ANGPD-2 , ANGPD-3 , ANGPD-4 , PDGF-A , PDGF-R , PDGF-D , EGF , FST , VEGF-A , VEGF-C, and TGF in visfatin-treated chondrosarcoma cells ( Figure 2 a).…”

Section: Resultsmentioning

confidence: 99%

“…Importantly, researchers have reported finding increased levels of visfatin in chondrosarcoma cartilage [ 7 , 8 ]; visfatin expression increases with higher grades of chondrosarcoma, with the highest levels of visfatin found in grade III (poorly differentiated) disease. Visfatin promotes angiogenesis activity in endothelial cells and cancer cells and also chondrosarcoma metastasis [ 9 ]. We therefore sought to determine the relationships between visfatin and chondrosarcoma angiogenesis in cellular and preclinical experiments.…”

Section: Introductionmentioning

confidence: 99%

Visfatin-Induced Inhibition of miR-1264 Facilitates PDGF-C Synthesis in Chondrosarcoma Cells and Enhances Endothelial Progenitor Cell Angiogenesis

Song

Chang

Lin

et al. 2022

Cells

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New treatments for chondrosarcoma are extremely important. Chondrosarcoma is a primary malignant bone tumor with a very unfavorable prognosis. High-grade chondrosarcoma has a high potential to metastasize to any organ in the body. Platelet-derived growth factor (PDGF) is a potent angiogenic factor that promotes tumor angiogenesis and metastasis. The adipocytokine visfatin promotes metastatic potential of chondrosarcoma; however, the role of visfatin in angiogenesis in human chondrosarcoma is unclear. We report that the levels of PDGF-C expression were positively correlated with tumor stages, significantly higher than the levels of expression in normal cartilage. Visfatin increased PDGF-C expression and endothelial progenitor cell (EPC) angiogenesis through the PI3K/Akt/mTOR signaling pathway, and dose-dependently down-regulated the synthesis of miR-1264, which targets the 3′-UTR of PDGF-C. Additionally, we discovered inhibition of visfatin or PDGF-C in chondrosarcoma tumors significantly reduced tumor angiogenesis and size. Our results indicate that visfatin inhibits miR-1264 production through the PI3K/Akt/mTOR signaling cascade, and thereby promotes PDGF-C expression and chondrosarcoma angiogenesis. Visfatin may be worth targeting in the treatment of chondrosarcoma angiogenesis.

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“…Cell lysates were collected using a reporter lysis buffer and luciferase assay substrate. Luciferase activity was determined by our established protocol 31 …”

Section: Methodsmentioning

confidence: 99%

Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α₂β₁ expression

Tai

Wang

Swain

et al. 2022

Journal of Pineal Research

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Advanced prostate cancer often develops into bone metastasis, which is characterized by aberrant bone formation with chronic pain and lower chances of survival. No treatment exists as yet for osteoblastic bone metastasis in prostate cancer. The indolamine melatonin (N‐acetyl‐5‐methoxytryptamine) is a major regulator of the circadian rhythm. Melatonin has shown antiproliferative and antimetastatic activities but has not yet been shown to be active in osteoblastic bone lesions of prostate cancer. Our study investigations reveal that melatonin concentration‐dependently decreases the migratory and invasive abilities of two osteoblastic prostate cancer cell lines by inhibiting FAK, c‐Src, and NF‐κB transcriptional activity via the melatonin MT1 receptor, which effectively inhibits integrin α2β1 expression. Melatonin therapy appears to offer therapeutic possibilities for reducing osteoblastic bone lesions in prostate cancer.

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Visfatin Promotes the Metastatic Potential of Chondrosarcoma Cells by Stimulating AP-1-Dependent MMP-2 Production in the MAPK Pathway

Cited by 15 publications

References 43 publications

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

Visfatin-Induced Inhibition of miR-1264 Facilitates PDGF-C Synthesis in Chondrosarcoma Cells and Enhances Endothelial Progenitor Cell Angiogenesis

Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α₂β₁ expression

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Visfatin Promotes the Metastatic Potential of Chondrosarcoma Cells by Stimulating AP-1-Dependent MMP-2 Production in the MAPK Pathway

Cited by 15 publications

References 43 publications

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

Visfatin increases the invasive potential of ovarian granulosa tumor spheroids by reprogramming glucose metabolism

Visfatin-Induced Inhibition of miR-1264 Facilitates PDGF-C Synthesis in Chondrosarcoma Cells and Enhances Endothelial Progenitor Cell Angiogenesis

Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α2β1 expression

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Melatonin suppresses the metastatic potential of osteoblastic prostate cancers by inhibiting integrin α₂β₁ expression