Corticotropin Releasing Hormone and Urocortin 3 Stimulate Vascular Endothelial Growth Factor Expression through the cAMP/CREB Pathway

Rhee, Sang Hoon; Elise, L.; Lee, Yunna; Taché, Yvette; Pothoulakis, Charalabos

doi:10.1074/jbc.m115.678979

Cited by 16 publications

(7 citation statements)

References 52 publications

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“…CRH and CRHR1 have also been reported to promote VEGF expression and inflammatory angiogenesis . The role of CRH in tumor angiogenesis in colon cancer is still unknown.…”

Section: Discussionmentioning

confidence: 99%

“…VEGF signaling in tumor affects tumor initiation and progression and that this is dependent of VEGF‐mediated angiogenesis and vascular permeability . It has been reported that CRH modulates VEGF expression in intestinal epithelial cells and CRHR1 mediates the angiogenesis in colitis by promoting VEGF expression . Whereas the role of CRH/CRHR1 signaling in angiogenesis of colon cancer is still unclear.…”

Section: Introductionmentioning

confidence: 99%

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CRH promotes human colon cancer cell proliferation via IL‐6/JAK2/STAT3 signaling pathway and VEGF‐induced tumor angiogenesis

Fang

Hong

Dai

et al. 2017

Molecular Carcinogenesis

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Corticotrophin-releasing hormone (CRH) has been demonstrated to participate in various diseases. Our previous study showed that its receptor CRHR1 mediated the development of colitis-associated cancer in mouse model. However, the detailed mechanisms remain unclear. In this study, we explored the oncogenetic role of CRH/CRHR1 signaling in colon cancer cells. Cell proliferation and colony formation assays revealed that CRH contributed to cell proliferation. Moreover, tube formation assay showed that CRH-treated colon cancer cell supernatant significantly promoted tube formation of human umbilical vein endothelial cells (HUVECs). And these effects could be reversed by the CRHR1 specific antagonist Antalarmin. Further investigation showed that CRH significantly upregulated the expressions of interlukin-6 (IL-6) and vascular endothelial growth factor (VEGF) through activating nuclear factor-kappa B (NF-κB). The CRH-induced IL-6 promoted phosphorylation of janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). STAT3 inhibition by Stattic significantly inhibited the CRH-induced cell proliferation. In addition, silence of VEGF resulted in declined tube formation induced by CRH. Taken together, CRH/CRHR1 signaling promoted human colon cancer cell proliferation via NF-κB/IL-6/JAK2/STAT3 signaling pathway and tumor angiogenesis via NF-κB/VEGF signaling pathway. Our results provide evidence to support a critical role for the CRH/CRHR1 signaling in colon cancer progression and suggest its potential utility as a new therapeutic target for colon cancer.

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“…CRH and CRHR1 have also been reported to promote VEGF expression and inflammatory angiogenesis . The role of CRH in tumor angiogenesis in colon cancer is still unknown.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CRH promotes human colon cancer cell proliferation via IL‐6/JAK2/STAT3 signaling pathway and VEGF‐induced tumor angiogenesis

Fang

Hong

Dai

et al. 2017

Molecular Carcinogenesis

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“…3a, 4d). Both, Egr1 and Creb1 have been implicated in several pro-angiogenic pathways and blood flow recovery after HLI 18,50,52,53 . To determine whether Mapk10 mediates Egr1 protein expression in neural cell lines, we utilized immunostaining for Egr1 after Mapk10 knockdown N2a cells.…”

Section: Resultsmentioning

confidence: 99%

Neural JNK3 regulates blood flow recovery after hindlimb ischemia in mice via an Egr1/Creb1 axis

et al. 2019

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Diseases related to impaired blood flow such as peripheral artery disease (PAD) impact nearly 10 million people in the United States alone, yet patients with clinical manifestations of PAD (e.g., claudication and limb ischemia) have limited treatment options. In ischemic tissues, stress kinases such as c-Jun N-terminal kinases (JNKs), are activated. Here, we show that inhibition of the JNK3 (Mapk10) in the neural compartment strikingly potentiates blood flow recovery from mouse hindlimb ischemia. JNK3 deficiency leads to upregulation of growth factors such as Vegfa, Pdgfb, Pgf, Hbegf and Tgfb3 in ischemic muscle by activation of the transcription factors Egr1/Creb1. JNK3 acts through Forkhead box O3 (Foxo3a) to suppress the activity of Egr1/Creb1 transcription regulators in vitro. In JNK3-deficient cells, Foxo3a is suppressed which leads to Egr1/Creb1 activation and upregulation of downstream growth factors. Collectively, these data suggest that the JNK3-Foxo3a-Egr1/Creb1 axis coordinates the vascular remodeling response in peripheral ischemia.

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“…Numerous previous studies have described the regulation of VEGFA gene expression. Many transcription factors have been identified as VEGF-positive and -negative regulators, including hypoxia-inducible factor 1 subunit alpha (HIF1a) [ 10 , 11 ], Sp transcription factors [ 12 ], NF-κB [ 13 ], SMAD [ 14 ], SRY-box transcription factor 9 (SOX9) [ 15 ], forkhead box O3 (FOXO3) [ 16 , 17 ], signal transducer and activator of transcription 3 (STAT3) [ 18 , 19 ], cAMP responsive element binding protein 1 (CREB1) [ 20 ], and AP-1 transcription factors [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. In recent years, research has focused on the function of AP-1 factors in endothelial cells.…”

Section: Vascular Endothelial Cells and Activator Protein 1 (Ap-1)mentioning

confidence: 99%

Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

Yoshitomi

Ikeda

Saito-Takatsuji

et al. 2021

IJMS

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Blood vessels are essential for the formation and maintenance of almost all functional tissues. They play fundamental roles in the supply of oxygen and nutrition, as well as development and morphogenesis. Vascular endothelial cells are the main factor in blood vessel formation. Recently, research findings showed heterogeneity in vascular endothelial cells in different tissue/organs. Endothelial cells alter their gene expressions depending on their cell fate or angiogenic states of vascular development in normal and pathological processes. Studies on gene regulation in endothelial cells demonstrated that the activator protein 1 (AP-1) transcription factors are implicated in angiogenesis and vascular development. In particular, it has been revealed that JunB (a member of the AP-1 transcription factor family) is transiently induced in endothelial cells at the angiogenic frontier and controls them on tip cells specification during vascular development. Moreover, JunB plays a role in tissue-specific vascular maturation processes during neurovascular interaction in mouse embryonic skin and retina vasculatures. Thus, JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development. In this review, we discuss the recently identified role of JunB in endothelial cells and blood vessel formation.

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Corticotropin Releasing Hormone and Urocortin 3 Stimulate Vascular Endothelial Growth Factor Expression through the cAMP/CREB Pathway

Cited by 16 publications

References 52 publications

CRH promotes human colon cancer cell proliferation via IL‐6/JAK2/STAT3 signaling pathway and VEGF‐induced tumor angiogenesis

CRH promotes human colon cancer cell proliferation via IL‐6/JAK2/STAT3 signaling pathway and VEGF‐induced tumor angiogenesis

Neural JNK3 regulates blood flow recovery after hindlimb ischemia in mice via an Egr1/Creb1 axis

Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development

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