Angiotensin II Type 1 Receptor Expression in Human Gastric Cancer and Induces MMP2 and MMP9 Expression in MKN-28 Cells

Huang, Wei; Yu, Li; Zhong, Jie; Qiao, Mingqi; Jiang, Feng-Xiang; Du, Fang; Tian, Xianglong; Wu, Yun

doi:10.1007/s10620-007-9838-9

Cited by 30 publications

(30 citation statements)

References 18 publications

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“…Previous cancer studies have demonstrated that AngII augments the migration and invasion of choriocarcinoma cells through the AT1R and induces MMP-2 and MMP-9 expression in gastric cancer cells (25)(26)(27). Consistent with these effects of AngII, we showed that treatment with AngII significantly increases the invasive ability of A549 lung cancer cells.…”

Section: Discussionsupporting

confidence: 89%

Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro

Wan

2011

Oncol Rep

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Abstract. Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensinconverting enzyme 2 (ACE2) is a newly identified component of RAS. The role of AngII and ACE2 in the metastasis of non-small cell lung cancer (NSCLC) and the effects on matrix metalloproteinases (MMPs) are still unknown. In the present study, the anti-invasive effect and mechanism of ACE2 were investigated in vitro and in vivo. Results of a transwell assay showed that the overexpression of ACE2 reduces the invasive ability of A549 cells in vitro. According to the results of qRT-PCR and Western blot analysis, the inhibitory role of ACE2 was mediated through the down-regulation of MMP-2 and MMP-9. Additionally, we confirmed that the overexpression of ACE2 inhibited cell growth and VEGFa production while simultaneously suppressing ACE and angiotensin II type 1 receptor (AT1R) expression in human lung cancer xenografts. These results suggest that the overexpression of ACE2 may potentially suppress the invasion and angiogenesis of NSCLC.

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Section: Discussionsupporting

confidence: 89%

Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro

Wan

2011

Oncol Rep

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“…Regarding histologic localization of the AT1 receptor, immunoreactivity was evident in membranous and cytoplasmic patterns. This is in accordance with findings described by Huang et al (18).…”

Section: At1 Expression In Human Gastric Cancer Cell Lines and Tissuessupporting

confidence: 94%

“…This study also showed AT1 receptor protein was overexpressed immnohistochemically in pancreatic ductal cancer cells, whereas the colon cancer cells had extremely weak or negative immunoreactivity for AT1 receptor (7). In gastric caner, it has been also reported that AT1 receptor is overexpressed in cancer tissues (18)(19)(20)(21), little information exists on the local synthesis of angiotensin II. Classically, the physiological activity of angiotensin II has long been recognized to be dependent on conversion of its precursor angiotensin I by angiotensin-converting enzyme (ACE).…”

Section: Discussionmentioning

confidence: 54%

“…With respect to gastric cancer, several studies have been reported on the local expression of AT1 receptor and have suggested that angiotensin II could play a key factor in tumor growth and metastatic spread via the AT1 receptor (18)(19)(20)(21). These data might indicate that a local tissue RAS is present and is potentially able to supply angiotensin II to the receptors in gastric cancer tissues.…”

Section: Introductionmentioning

confidence: 99%

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Local angiotensin II-generation in human gastric cancer: Correlation with tumor progression through the activation of ERK1/2, NF-κB and survivin

Koyama

Fushida²,

Harada³

et al. 2009

Int J Oncol

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Abstract. Angiotensin II is a main effector peptide in renin-angiotensin system, acting as a growth promoter via angiotensin II type 1 (AT1) receptor. The present study examined intrinsic angiotensin II generating system in gastric cancer and potential roles of angiotensin II in cellular proliferation and survival. The expression of AT1 receptor was examined in gastric cancer cell lines and tissues. In addition, we measured angiotensin II concentration in tissues from twenty gastric cancer and corresponding normal region using the florisil method. In vitro, we investigated the potential roles of angiotensin II in cellular proliferation and cell survival in cultured human gastric cancer cell line. The effects of AT1 receptor blocker candesartan were evaluated in a mouse model of peritoneal carcinomatosis. AT1 receptor protein was expressed in gastric cancer cell lines and tissues. Angiotensin II concentration in tumor region (1447±624 pg/g wet) was significantly higher than those of normal region (775±320 pg/g wet) (p<0.05). Angiotensin II stimulates the cell proliferation in the AT1 receptor-positive OCUM2MD3 gastric cancer cell line and this proliferative effect of angiotensin II was inhibited by a specific AT1 receptor antagonist, candesartan. We also confirmed the angiotensin II stimulated ERK1/2, nuclear transcript factor-κB (NF-κB) and surviving activation, which are central molecules of cellular proliferation and survival in OCUM2MD3 cells. Candesartan significantly prolonged survival time in a mouse model of peritoneal carcinomatosis compared with control group (p=0.0.197, log-rank test). Our data provide in vivo evidence of intrinsic angiotensin II generating system in gastric cancer and indicate locally formed angiotensin II is involved in cellular proliferation and survival.

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“…Members of the MMP family, in particular, MMP-9, are associated with regulation of cancer cell invasion and metastasis, the most insidious and life-threating aspects of cancer (21,22). Therefore, the development of compounds capable of inhibiting MMP-9 could prove invaluable in the treatment of breast cancer patients.…”

Section: Discussionmentioning

confidence: 99%

Shikonin blocks migration and invasion of human breast cancer cells through inhibition of matrix metalloproteinase-9 activation

et al. 2014

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Abstract. Shikonin, a natural naphthoquinone isolated from a traditional Chinese medicinal herb, has been reported to promote tumor cell death. However, there are few reports concerning its effect on metastasis-related cell invasion and migration behavior. In the present study, we investigated the effect of shikonin on human breast cancer invasion and migration. We found that shikonin inhibited phorbol 12-myristate 13-acetate (PMA)-induced cell migration and invasion in MCF-7 breast cancer cells, which was correlated with modulation of matrix metalloproteinase-9 (MMP-9) through suppression of both expression and proteolytic and promoter activity. We also found that shikonin inhibited both MMP-9 expression and promoter activity in MDA-MB-231 cells with high metastatic potential. These results indicated that shikonin induces the suppression of migration and invasion through modulation of MMP-9 in human breast cancer cells. Therefore, shikonin may be a potential anticancer drug for human breast cancer therapy. IntroductionBreast cancer ranks among the most common malignant tumors afflicting women worldwide (1). Cancer metastasis is the leading cause of mortality in patients with breast cancer; breast cancer survival rates fall from 90% for localized to 20% for metastatic disease. Therefore, controlling metastasis and invasion represents an important therapeutic strategy (2). Metastasis requires that invasive cells detach from localized tumors by degrading the extracellular matrix using proteases, including matrix metalloproteinases (MMPs); survive in the circulation as circulating tumor cells (CTCs); and colonize distant locations. Thus, understanding the molecular mechanisms underlying each of these steps is essential for targeting metastatic cells at an early stage and improving patient survival (3).MMPs are a family of extracellular matrix (ECM)-degrading enzymes comprising 24 members. Based on their substrates, MMPs are divided into four subclasses: collagenase, gelatinase, stromelysin and membrane-associated (4). As a main ECM-degrading enzyme family, MMPs have essential roles in physiologic processes such as tissue development, remodeling and wound healing (5). However, they are also involved in certain tissue destructive diseases, such as atherosclerosis, inflammation, rheumatoid arthritis, and tumor invasion, metastasis and neoangiogenesis (6). Recent studies have shown that MMPs are important elements of the tumor microenvironment, regulating tumor progression, metastatic niche formation and inflammation in cancer (7). Among human MMPs, MMP-2 (gelatinase-A) and MMP-9 (gelatinase-B) are key enzymes in the degradation of type IV collagen, which is an important component of the ECM. MMP-2 and MMP-9 are the MMP members primarily associated with tumor migration, invasion and metastasis of various types of cancers (8). It has been shown that enhanced expression of MMP-9 is associated with the progression and invasion of tumors, whereas MMP-2 is usually expressed constitutively (9,10). Thus, researchers have focu...

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Angiotensin II Type 1 Receptor Expression in Human Gastric Cancer and Induces MMP2 and MMP9 Expression in MKN-28 Cells

Cited by 30 publications

References 18 publications

Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro

Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro

Local angiotensin II-generation in human gastric cancer: Correlation with tumor progression through the activation of ERK1/2, NF-κB and survivin

Shikonin blocks migration and invasion of human breast cancer cells through inhibition of matrix metalloproteinase-9 activation

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