Anterior gradient 2: A new target to treat colorectal cancer

Gao, Hua; Xu, Xiao; Chen, Bing; Wang, Feng; Zhang, Wenbin; Geng, Hongzhi; Wang, Yunhai

doi:10.1016/j.mehy.2013.02.015

Cited by 8 publications

(7 citation statements)

References 25 publications

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“…[21][22][23][24][25]31 In this study, the effect of rhES-AuNPs on mCRC tumor growth in vivo was firstly evaluated. The results suggested that rhES-AuNPs experimental group could modulate vascular morphology in mCRC tumor and improve tumor hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…As a new antitumor strategy, vascular normalization induced by antiangiogenic therapy was widely studied in the treatment of tumor, but for AGR2 over-expressed malignant tumors, the influence of rhES-AuNPs on the expression or the function of AGR2 was not elucidated. [21][22][23][24][25]31 In this study, the effect of rhES-AuNPs on mCRC tumor growth in vivo was firstly evaluated. The results suggested that rhES-AuNPs experimental group could modulate vascular morphology in mCRC tumor and improve tumor hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…23 However, it is assumed that the role of AGR2 is necessary in the metastatic progression in CRC, and AGR2 may also be an impactful target for metastatic colorectal cancer (mCRC) treatment. 24 Indeed, previous studies show that AGR2 over-expressed in SW620, which was one kind of mCRC cells. 25 Overall, tumor angiogenesis is an extremely complex process, which covers a multitude of underlying TAFs.…”

Section: Introductionmentioning

confidence: 97%

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Conjugation of gold nanoparticles and recombinant human endostatin modulates vascular normalization via interruption of anterior gradient 2–mediated angiogenesis

Fan

Yang

et al. 2017

Tumour Biol.

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Several studies have revealed the potential of normalizing tumor vessels in anti-angiogenic treatment. Recombinant human endostatin is an anti-angiogenic agent which has been applied in clinical tumor treatment. Our previous research indicated that gold nanoparticles could be a nanoparticle carrier for recombinant human endostatin delivery. The recombinant human endostatin-gold nanoparticle conjugates normalized vessels, which improved chemotherapy. However, the mechanism of recombinant human endostatin-gold nanoparticle-induced vascular normalization has not been explored. Anterior gradient 2 has been reported to be over-expressed in many malignant tumors and involved in tumor angiogenesis. To date, the precise efficacy of recombinant human endostatin-gold nanoparticles on anterior gradient 2-mediated angiogenesis or anterior gradient 2-related signaling cohort remained unknown. In this study, we aimed to explore whether recombinant human endostatin-gold nanoparticles could normalize vessels in metastatic colorectal cancer xenografts, and we further elucidated whether recombinant human endostatin-gold nanoparticles could interrupt anterior gradient 2-induced angiogenesis. In vivo, it was indicated that recombinant human endostatingold nanoparticles increased pericyte expression while inhibit vascular endothelial growth factor receptor 2 and anterior gradient 2 expression in metastatic colorectal cancer xenografts. In vitro, we uncovered that recombinant human endostatin-gold nanoparticles reduced cell migration and tube formation induced by anterior gradient 2 in human umbilical vein endothelial cells. Treatment with recombinant human endostatin-gold nanoparticles attenuated anterior gradient 2-mediated activation of MMP2, cMyc, VE-cadherin, phosphorylation of p38, and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in human umbilical vein endothelial cells. Our findings demonstrated recombinant human endostatin-gold nanoparticles might normalize vessels by interfering anterior gradient 2-mediated angiogenesis in metastatic colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Conjugation of gold nanoparticles and recombinant human endostatin modulates vascular normalization via interruption of anterior gradient 2–mediated angiogenesis

Fan

Yang

et al. 2017

Tumour Biol.

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“…AGR2 has been reported to be overexpressed in several adenocarcinomas, including breast (5), colorectal (6), ��g��l (7), l��g (8), ��c��c (9) �� (10,11) carcinomas. ARG2 is considered to promote cell proliferation, cell survival and the metastasis of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Expression of AGR2 in pituitary adenomas and its association with tumor aggressiveness

Tohti

et al. 2015

Oncology Letters

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“… 15 AGR2 is a novel target for the treatment of colorectal cancer and its high expression in colon cancer modulates cell function. 16 In addition, AGR2 is highly expressed in esophageal cancer, 17 pancreatic cancer, 18 prostate cancer, 19 and lung cancer. 20 , 21 ARG2 is thought to promote proliferation, survival, and metastasis of tumor cells.…”

Section: Introductionmentioning

confidence: 99%

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

He¹,

Fu²,

Hu³

et al. 2021

CMAR

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Objective Studies have indicated that AGR2 is crucial in many cancers. However, its methylation level in lung adenocarcinoma (LUAD) is rarely known. Hence, the effect of AGR2 methylation on LUAD was explored in the study. Methods qRT-PCR was adopted to detect the expression of AGR2 in LUAD cells and normal lung cells. Methylation-specific PCR (MSP) was used to detect the methylation of AGR2 promoter region in different cell lines. MTT, Transwell and wound healing assays were used to verify the progression of cells in each transfection group. Results The expression of AGR2 was significantly up-regulated in LUAD cells relative to that in normal cells. Moreover, the expression of AGR2 was inversely modulated by DNA methylation, and the hypomethylation of CpG islands would lead to the increased expression of AGR2. Finally, overexpression and hypomethylation of AGR2 facilitated the proliferation, invasion and migration of LUAD cells. Conclusion These results demonstrated that hypomethylation of AGR2 promoter region promoted the expression of AGR2 in LUAD cells, thus promoting the progression of LUAD cells.

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Anterior gradient 2: A new target to treat colorectal cancer

Cited by 8 publications

References 25 publications

Conjugation of gold nanoparticles and recombinant human endostatin modulates vascular normalization via interruption of anterior gradient 2–mediated angiogenesis

Conjugation of gold nanoparticles and recombinant human endostatin modulates vascular normalization via interruption of anterior gradient 2–mediated angiogenesis

Expression of AGR2 in pituitary adenomas and its association with tumor aggressiveness

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

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