Gastrin promotes angiogenesis by activating HIF-1α/β-catenin/VEGF signaling in gastric cancer

Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17...

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Published in:	Gene Vol. 704; pp. 42 - 48
Main Authors:	Tang, E., Wang, Yongfeng, Liu, Tiemei, Yan, Bin
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01.07.2019
Subjects:	Angiogenesis beta catenin cell proliferation Gastric cancer Gastrin gastrins hypoxia hypoxia-inducible factor 1 in vivo studies metastasis neoplasm progression normoxia stomach neoplasms vascular endothelial growth factors VEGF β-Catenin Angiogenesis COX-2 VEGF Gastrin β-Catenin GC G17 MTT Gastric cancer
ISSN:	0378-1119, 1879-0038, 1879-0038
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Abstract	Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17 (G17) increased the proliferation of AGS cells and enhanced tube formation during normoxia and hypoxia. The expression level of VEGF were increased by G17 treatment as well. Experiments on the mechanism showed that G17 promoted HIF-1α expression, which subsequently enhanced β-catenin nuclear localization and activation of TCF3 and LEF1 and finally resulted in angiogenesis by upregulating VEGF. An in vivo experiment confirmed that G17 enhanced GC cell proliferation and angiogenesis in the resultant tumor. In conclusion, our findings indicate that gastrin promotes angiogenesis via activating HIF-1α/β-catenin/VEGF axis in GC. •Gastrin promotes proliferation of GC cells and angiogenesis under normoxic and hypoxic conditions.•Gastrin promotes angiogenesis through the β-catenin/VEGF pathway in the normoxic condition.•Gastrin promotes angiogenesis via the HIF-1α/β-catenin/VEGF pathway under hypoxia.•Gastrin promotes GC cell proliferation and angiogenesis during hypoxia in vivo.
AbstractList	Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17 (G17) increased the proliferation of AGS cells and enhanced tube formation during normoxia and hypoxia. The expression level of VEGF were increased by G17 treatment as well. Experiments on the mechanism showed that G17 promoted HIF-1α expression, which subsequently enhanced β-catenin nuclear localization and activation of TCF3 and LEF1 and finally resulted in angiogenesis by upregulating VEGF. An in vivo experiment confirmed that G17 enhanced GC cell proliferation and angiogenesis in the resultant tumor. In conclusion, our findings indicate that gastrin promotes angiogenesis via activating HIF-1α/β-catenin/VEGF axis in GC. •Gastrin promotes proliferation of GC cells and angiogenesis under normoxic and hypoxic conditions.•Gastrin promotes angiogenesis through the β-catenin/VEGF pathway in the normoxic condition.•Gastrin promotes angiogenesis via the HIF-1α/β-catenin/VEGF pathway under hypoxia.•Gastrin promotes GC cell proliferation and angiogenesis during hypoxia in vivo. Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17 (G17) increased the proliferation of AGS cells and enhanced tube formation during normoxia and hypoxia. The expression level of VEGF were increased by G17 treatment as well. Experiments on the mechanism showed that G17 promoted HIF-1α expression, which subsequently enhanced β-catenin nuclear localization and activation of TCF3 and LEF1 and finally resulted in angiogenesis by upregulating VEGF. An in vivo experiment confirmed that G17 enhanced GC cell proliferation and angiogenesis in the resultant tumor. In conclusion, our findings indicate that gastrin promotes angiogenesis via activating HIF-1α/β-catenin/VEGF axis in GC. Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17 (G17) increased the proliferation of AGS cells and enhanced tube formation during normoxia and hypoxia. The expression level of VEGF were increased by G17 treatment as well. Experiments on the mechanism showed that G17 promoted HIF-1α expression, which subsequently enhanced β-catenin nuclear localization and activation of TCF3 and LEF1 and finally resulted in angiogenesis by upregulating VEGF. An in vivo experiment confirmed that G17 enhanced GC cell proliferation and angiogenesis in the resultant tumor. In conclusion, our findings indicate that gastrin promotes angiogenesis via activating HIF-1α/β-catenin/VEGF axis in GC.Angiogenesis is recognized as a sign of cancer and facilitates cancer progression and metastasis. Suppression of angiogenesis is a desirable strategy for gastric cancer (GC) management. In this study, we showed a novel role of gastrin in angiogenesis of GC. We observed that treatment with gastrin 17 (G17) increased the proliferation of AGS cells and enhanced tube formation during normoxia and hypoxia. The expression level of VEGF were increased by G17 treatment as well. Experiments on the mechanism showed that G17 promoted HIF-1α expression, which subsequently enhanced β-catenin nuclear localization and activation of TCF3 and LEF1 and finally resulted in angiogenesis by upregulating VEGF. An in vivo experiment confirmed that G17 enhanced GC cell proliferation and angiogenesis in the resultant tumor. In conclusion, our findings indicate that gastrin promotes angiogenesis via activating HIF-1α/β-catenin/VEGF axis in GC.
Author	Yan, Bin Liu, Tiemei Wang, Yongfeng Tang, E.
Author_xml	– sequence: 1 givenname: E. surname: Tang fullname: Tang, E. organization: Department of Gastroenterology, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, China – sequence: 2 givenname: Yongfeng surname: Wang fullname: Wang, Yongfeng organization: Department of General Surgery, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, China – sequence: 3 givenname: Tiemei surname: Liu fullname: Liu, Tiemei email: liu.tiemei@qphospital.com organization: Department of Gastroenterology, Endoscopy Center, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, China – sequence: 4 givenname: Bin surname: Yan fullname: Yan, Bin email: yan.bin@qphospital.com organization: Department of General Surgery, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, China
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Keywords	Angiogenesis COX-2 VEGF Gastrin β-Catenin GC G17 MTT Gastric cancer
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SubjectTerms	Angiogenesis beta catenin cell proliferation Gastric cancer Gastrin gastrins hypoxia hypoxia-inducible factor 1 in vivo studies metastasis neoplasm progression normoxia stomach neoplasms vascular endothelial growth factors VEGF β-Catenin
Title	Gastrin promotes angiogenesis by activating HIF-1α/β-catenin/VEGF signaling in gastric cancer
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