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内脂素诱导 miR-1264 抑制促进软骨肉瘤细胞 PDGF-C 的合成并增强内皮祖细胞血管生成。

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

机构信息

Graduate Institute of Biomedical Science, China Medical University, Taichung 404333, Taiwan.

Translational Medicine Center, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei City 111045, Taiwan.

出版信息

Cells. 2022 Nov 2;11(21):3470. doi: 10.3390/cells11213470.

DOI:10.3390/cells11213470
PMID:36359873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9656973/
Abstract

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.

摘要

软骨肉瘤的新治疗方法至关重要。软骨肉瘤是一种原发性恶性骨肿瘤，预后极差。高级别软骨肉瘤有向身体任何器官转移的高潜力。血小板衍生生长因子 (PDGF) 是一种有效的血管生成因子，可促进肿瘤血管生成和转移。脂肪细胞因子内脂素促进软骨肉瘤的转移潜力；然而，内脂素在人软骨肉瘤中的血管生成作用尚不清楚。我们报告称，PDGF-C 表达水平与肿瘤分期呈正相关，明显高于正常软骨中的表达水平。内脂素通过 PI3K/Akt/mTOR 信号通路增加 PDGF-C 表达和内皮祖细胞 (EPC) 血管生成，并呈剂量依赖性地下调靶向 PDGF-C 3'UTR 的 miR-1264 的合成。此外，我们发现软骨肉瘤肿瘤中内脂素或 PDGF-C 的抑制显著减少了肿瘤血管生成和大小。我们的结果表明，内脂素通过 PI3K/Akt/mTOR 信号级联抑制 miR-1264 的产生，从而促进 PDGF-C 表达和软骨肉瘤血管生成。内脂素在治疗软骨肉瘤血管生成方面可能值得关注。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/069970fa394f/cells-11-03470-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/3e5ff1c02105/cells-11-03470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/cafeccb3af75/cells-11-03470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/540a6b3292d0/cells-11-03470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/8d3b206bf901/cells-11-03470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/1fc873191ead/cells-11-03470-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/43c39115cd5d/cells-11-03470-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/069970fa394f/cells-11-03470-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/3e5ff1c02105/cells-11-03470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/cafeccb3af75/cells-11-03470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/540a6b3292d0/cells-11-03470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/8d3b206bf901/cells-11-03470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/1fc873191ead/cells-11-03470-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/43c39115cd5d/cells-11-03470-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce00/9656973/069970fa394f/cells-11-03470-g007.jpg

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