Tumor angiogenesis of SCLC inhibited by decreased expression of FMOD via downregulating angiogenic factors of endothelial cells

Ao, Zhi; Yu, Shilong; Pei, Qian; Gao, Wenhong; Guo, Ruiling; Dong, Xiaoxiao; Xu, Jun; Zhang, Ruijie; Jiang, Chaowen; Ji, Fuyun; Qian, Guisheng

doi:10.1016/j.biopha.2016.12.110

Cited by 31 publications

(34 citation statements)

References 33 publications

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“…FMOD plays an important role in angiogenesis in lung cancer and in cutaneous and optical diseases associated with angiogenesis and wound healing [ 14 , 15 , 28 ]. In addition, a previous study has shown that FMOD is highly expressed in human glioblastoma and is upregulated by TGF-β via the demethylation of its promoter in glioblastoma cells [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Glial Cell Line-Derived Neurotrophic Factor (GDNF) Promotes Angiogenesis through the Demethylation of the Fibromodulin (FMOD) Promoter in Glioblastoma

Chen

Lü

et al. 2018

Med Sci Monit

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BackgroundAngiogenesis plays an important role in the progression of glioblastoma, with a high degree of malignancy. Previous studies have proved that glial cell line-derived neurotrophic factor (GDNF) and fibromodulin (FMOD) are strongly expressed in human glioblastoma. The purpose of this study was to explore the roles of GDNF and FMOD in angiogenesis and the molecular mechanisms underlying these roles in human glioblastoma.Material/MethodsThe effects of GDNF on the expression and secretion of vascular endothelial growth factor (VEGF) in human glioblastoma cell line U251 and angiogenesis in human umbilical vein endothelial cells (HUVECs) were investigated. The molecular mechanism of GDNF-induced expression of FMOD was explored. The roles of FMOD in GDNF-induced expression and secretion of VEGF and angiogenesis were also examined.ResultsIn the present study, we showed that GDNF promoted the expression and secretion of VEGF in U251 cells. VEGF mediated GDNF-induced angiogenesis in human glioblastoma. In addition, GDNF significantly upregulated the expression of FMOD in U251 cells. Mechanistically, the results of luciferase reporter assay and methylation-specific PCR (MSP) demonstrated that GDNF facilitated the demethylation of the FMOD promoter. More importantly, we found that FMOD acted as an important mediator in VEGF expression and angiogenesis induced by GDNF in human glioblastoma.ConclusionsCollectively, our data show that GDNF promotes angiogenesis through demethylation of the FMOD promoter in human glioblastoma, indicating that GDNF and FMOD may be potential therapeutic targets for glioblastoma.

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Section: Discussionmentioning

confidence: 99%

Glial Cell Line-Derived Neurotrophic Factor (GDNF) Promotes Angiogenesis through the Demethylation of the Fibromodulin (FMOD) Promoter in Glioblastoma

Chen

Lü

et al. 2018

Med Sci Monit

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“…Angiogenesis is a vital step in the physiological process of tissue repair and regeneration, bone remodeling and reproduction, and embryonic development (Folkman, 2006;Garona et al, 2018;Annese et al, 2019). Moreover, it also played a critical role in the progression of tumor formation, infiltration, invasion, and metastasis (Carmeliet, 2006;Seano et al, 2014;Lii et al, 2016;Ao et al, 2017;Yang et al, 2017). Thus, inhibition of angiogenesis has become an effective strategy for cancer therapy.…”

Section: Tan Iia Inhibits Tumor Angiogenesismentioning

confidence: 99%

The Anticancer Properties of Tanshinones and the Pharmacological Effects of Their Active Ingredients

Han

Zhou

et al. 2020

Front. Pharmacol.

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Cancer is a common malignant disease worldwide with an increasing mortality in recent years. Salvia miltiorrhiza, a well-known traditional Chinese medicine, has been used for the treatment of cardiovascular and cerebrovascular diseases for thousands of years. The liposoluble tanshinones in S. miltiorrhiza are important bioactive components and mainly include tanshinone IIA, dihydrodanshinone, tanshinone I, and cryptotanshinone. Previous studies showed that these four tanshinones exhibited distinct inhibitory effects on tumor cells through different molecular mechanisms in vitro and in vivo. The mechanisms mainly include the inhibition of tumor cell growth, metastasis, invasion, and angiogenesis, apoptosis induction, cell autophagy, and antitumor immunity, and so on. In this review, we describe the latest progress on the antitumor functions and mechanisms of these four tanshinones to provide a deeper understanding of the efficacy. In addition, the important role of tumor immunology is also reviewed.

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“…A previous study conducted by Zhang et al () has demonstrated that downregulation of miR‐502‐5p reduces injury and apoptosis of chondrocytes in OA with an increase in cell viability by the negative targeting of the TRAF2 gene through inhibition of the NF‐κB signaling pathway. A previous study found that the decreased secretion of FMOD could inhibit the proliferation, migration, and invasion of human umbilical vessel endothelial cells through downregulation of several growth factors (Ao et al, ). Therefore, we may infer that the downregulation of miR‐340‐5p inhibits apoptosis of chondrocytes in OA by negatively targeting FMOD through the ERK signaling pathway.…”

Section: Discussionmentioning

confidence: 98%

Downregulated microRNA‐340‐5p promotes proliferation and inhibits apoptosis of chondrocytes in osteoarthritis mice through inhibiting the extracellular signal‐regulated kinase signaling pathway by negatively targeting the FMOD gene

Zhang

Peng

et al. 2018

Journal Cellular Physiology

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Tumor angiogenesis of SCLC inhibited by decreased expression of FMOD via downregulating angiogenic factors of endothelial cells

Cited by 31 publications

References 33 publications

Glial Cell Line-Derived Neurotrophic Factor (GDNF) Promotes Angiogenesis through the Demethylation of the Fibromodulin (FMOD) Promoter in Glioblastoma

Glial Cell Line-Derived Neurotrophic Factor (GDNF) Promotes Angiogenesis through the Demethylation of the Fibromodulin (FMOD) Promoter in Glioblastoma

The Anticancer Properties of Tanshinones and the Pharmacological Effects of Their Active Ingredients

Downregulated microRNA‐340‐5p promotes proliferation and inhibits apoptosis of chondrocytes in osteoarthritis mice through inhibiting the extracellular signal‐regulated kinase signaling pathway by negatively targeting the FMOD gene

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