Loss of angiotensin-converting enzyme 2 promotes growth of gallbladder cancer

Zong, Huajie; Yin, Baobing; Zhou, Huading; Cai, Duan; Ma, Baojin; Xiang, Yang

doi:10.1007/s13277-015-3171-2

Cited by 32 publications

(35 citation statements)

References 24 publications

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“…Our previous studies showed that the ACE2 overexpression inhibited cell growth and VEGF production in vivo (11,12). A recent study also showed that ACE2 suppressed tumor growth in gallbladder cancer (22). In the present study, we found that ACE2 overexpression inhibited the growth of A549-DDP tumor cells in vivo.…”

Section: Discussionsupporting

confidence: 78%

ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC

Cheng

Zhou

et al. 2016

Oncology Reports

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Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. We previously reported that ACE2 overexpression may inhibit cell growth and vascular endothelial growth factor (VEGF) production in vitro and in vivo. In the present study, we investigated the effect of ACE2 on tumor-associated angiogen-esis after the development of acquired platinum resistance in non-small cell lung cancer (NSCLC). Four NSCLC cell lines, A549, LLC, A549-DDP and LLC-DDP, were used in vitro, while A549 and A549-DDP cells were used in vivo. A549-DDP and LLC-DDP cells were newly established at our institution as acquired platinum-resistant sublines by culturing the former parent cells in cisplatin (CDDP)-containing conditioned medium for 6 months. These platinum-resistant cells showed significantly higher angiotensin II type 1 receptor (AT1R), ACE and VEGF production and lower ACE2 expression than their corresponding parent cells. We showed that ACE2 overexpression inhibited the production of VEGF in vitro and in vivo compared to their corresponding parent cells. We also found that ACE2 overexpression reduced the expression of AT1R and ACE. Additionally, we confirmed that ACE2 overexpres-sion inhibited cell growth and VEGF production while simultaneously suppressing ACE and AT1R expression in human lung cancer xenografts. Our findings indicate that ACE2 overexpression may potentially suppress angiogenesis in NSCLC after the development of acquired platinum resistance.

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Section: Discussionsupporting

confidence: 78%

ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC

Cheng

Zhou

et al. 2016

Oncology Reports

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“…Additionally, increased serum ACE2 activity has been reported in healthy individuals (Zong et al, 2015). Moreover, researchers have suggested that decreased ACE2 activity may reflect the presence of cancer associated with diabetes (Pedersen et al, 2015).…”

Section: Introductionmentioning

confidence: 97%

“…The ACE2/Ang-(1–7)/MasR axis, which represents a newly discovered component of the RAS, has been shown to be up-regulated or down-regulated in different cancers. Yu et al (2016) suggested that ACE2 expression is decreased in breast cancer, NSCLC (Feng et al, 2010), hepatocellular carcinoma (Ye et al, 2015), and pancreatic cancer (Zhou et al, 2009), and Zong et al (2015) reported that ACE2 levels are lower in gallbladder cancer cells than in normal gallbladder cells. Ang-(1–7) is generated primarily from Ang I or AngII via enzymatic cleavage; in recent studies, ACE2 has been identified as the main enzyme that generates Ang-(1–7), whereas ACE has been shown to be responsible for cleaving Ang-(1–7) to produce Ang-(1–5).…”

Section: Introductionmentioning

confidence: 99%

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The ACE2/Angiotensin-(1–7)/Mas Receptor Axis: Pleiotropic Roles in Cancer

Fan

et al. 2017

Front. Physiol.

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Cancer remains one of the most common causes of death and disability and represents a major economic burden in industrialized nations. The renin-angiotensin system (RAS) has been well-recognized as one of the most important regulators of both normal and pathological physiological processes in the brain, kidney, heart, and blood vessels. The activation of the angiotensin-converting enzyme 2/angiotensin-(1–7)/mitochondrial assembly receptor [ACE2/Ang-(1–7)/MasR] axis, which is one component of the RAS, has recently been identified as a critical component of pulmonary systems, gastric mucosa, and cancer. However, the ability of the ACE2/Ang-(1–7)/MasR axis to suppress or promote cancer has not been fully elucidated. In this review, we focus on recent experimental and clinical studies investigating the basic properties, roles, and mechanisms of ACE2, Ang-(1–7), and the MasR, as well as the axis pathway, to provide insights into possible therapeutic strategies for treating cancer that target the ACE2/Ang-(1–7)/MasR axis.

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“…Primary tumor site epithelial cells transform into mesenchymal cells through EMT, invading the basement membrane and transferring via blood vessels to form distant secondary tumor sites through MET ( 20 ). Microcircumstances have been considered important in tumor metastasis in previous years, and local RAS, which is expressed in the matrix, may be involved ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

AngII induces HepG2 cells to activate epithelial‑mesenchymal transition

Qi¹,

Zhou

Liu³

et al. 2018

Exp Ther Med

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The present study aimed to determine whether HepG2 can induce epithelial-mesenchymal transition (EMT) via angiotensin II (AngII) simulation. The expression levels of EMT markers vimentin and E-cadherin in cancer tissues and adjacent tissues of patients with hepatocellular carcinoma (HCC) were detected by immunohistochemistry. In addition, HepG2 cells were stimulated with AngII, and the gene and protein expression levels of vimentin and E-cadherin were measured by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively, whereas cell migration and invasion were assessed using Transwell assays. The AngII inhibitor Ang1-7 and the Ang1-7 inhibitor A779 were added to the system to further evaluate AngII-induced EMT. Compared with that in normal tissue, the expression level of vimentin in HCC tissue was increased, whereas that of E-cadherin was decreased. EMT occurred 48 h following AngII stimulation. The transcription level of E-cadherin in HepG2 cells was decreased, whereas that of vimentin was increased. In addition, the migration and invasion abilities of the cells were increased simultaneously. Ang1-7 partly inhibited AngII-induced EMT. When stimulated at an appropriate time, HepG2 cells have the ability to undergo EMT.

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Loss of angiotensin-converting enzyme 2 promotes growth of gallbladder cancer

Cited by 32 publications

References 24 publications

ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC

ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC

The ACE2/Angiotensin-(1–7)/Mas Receptor Axis: Pleiotropic Roles in Cancer

AngII induces HepG2 cells to activate epithelial‑mesenchymal transition

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