Similarities and differences between effects of angiotensin III and angiotensin II on human prostate cancer cell migration and proliferation

Domińska, Kamila; Piastowska-Ciesielska, Agnieszka Wanda; Lachowicz-Ochędalska, Agnieszka; Ochędalski, Tomasz

doi:10.1016/j.peptides.2012.07.022

Cited by 25 publications

(26 citation statements)

References 28 publications

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“…our earlier studies found that ang II significantly enhanced cell viability and proliferation in both prostate cancer cell lines (21,28). Uemura et al (29) found that AT1 receptor mRNA was strongly expressed in LNCaP cells and very poorly in PC3, which may explain the better response of the first line to angiotensin II-induced cell proliferation.…”

Section: Discussionmentioning

confidence: 91%

Interaction between angiotensin II and relaxin 2 in the progress of growth and spread of prostate cancer cells

Domińska

Ochędalski

Kowalska

et al. 2016

International Journal of Oncology

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Abstract. Deregulation of locally secreted hormones, such as angiotensin II (Ang II) and relaxin 2 (RLN2), has been linked to a higher risk of select cancers or a poor prognosis in patients. In this study, for the first time a common effect of Ang II and RLN2 in relation to various aspects of prostate cancer development and metastasis are presented. Four independent colorimetric assays were used to analyze cell viability and proliferation. The changes of cell adhesion to extracellular matrix proteins and invasion/aggressiveness ability of prostate cancer cells (LNCaP, PC3) before and after peptides treatment, were also investigated. The findings suggest that the both investigated systems, have an impact on cell growth/division or spread, to some degree via overlapping signal transduction pathways. Intermediate or sometimes poorer results were achieved by using a combination of both hormones than when each was used individually. It seems that Ang II and RLN2 can play a significant role in increasing the aggressiveness of prostate tumors by up-regulating BIRC5 expression and MMP-2 and MMP-9 secretion. In addition, we speculate that Ang II and RLN2 are involved in the transition from the androgen-dependent to the androgen-independent phenotype via modulation of the expression of androgen receptors.

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Section: Discussionmentioning

confidence: 91%

Interaction between angiotensin II and relaxin 2 in the progress of growth and spread of prostate cancer cells

Domińska

Ochędalski

Kowalska

et al. 2016

International Journal of Oncology

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“…Lysates from 184A1 cells were harvested and protein concentration was determined by the Bradford method (Bio-Rad, Poland) as described previously. 4,22,23 Protein extracts (30 µg) were denatured in Laemmli's sample buffer (bromophenol blue, 40% glycerol, 8-10% SDS, 20% β-mercaptoethanol), followed by 3 min heat denaturation at 100 o C.The samples were then resolved by SDS-PAGE on a 12.5% polyacrylamide gel. After electrophoresis (120 V for 2 h), proteins were transferred in transfer buffer to a PVDF membrane using constant current (400 mA for 70 min).…”

Section: Western Blot Analysismentioning

confidence: 99%

Angiotensin modulates human mammary epithelial cell motility

Piastowska-Ciesielska

Domińska

Nowakowska

et al. 2013

J Renin Angiotensin Aldosterone Syst

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Introduction: Angiotensin II is an effector peptide showing multiple physiological effects, such as regulation of vascular tone, tissue growth and remodelling. Postlactational involution of mammary gland involves changes such as high matrix metalloproteinase activity and release of bioactive fragments of fibronectin and laminin, which may be directly regulated by angiotensin II. The aim of the present study was to evaluate the influence of angiotensin II on proliferation, viability and motility of normal human mammary epithelial cells (184A1 cell line) and to determine the role of angiotensin II receptors in these processes. Materials and methods: Real-time reverse transcription-PCR, western blot and gelatin zymography were used to study the effect of angiotensin II on the expression of angiotensin receptors and matrix metalloproteinases in 184A1 cells. WST-1, AlamarBlue and BrdU assays were used as indicators of cell viability and proliferation after angiotensin II stimulation. Boyden chamber assays and monolayer wound migration assay were used to evaluate in vitro the changes in cell adhesion, migration and invasion. Results: Angiotensin II increased motility of the 184A1 cells and the ability of wound closure. Modifications in cell-substrate adhesion systems and increased secretion and activity of matrix metalloproteinases were also observed. The effect of angiotensin II was abolished by blocking angiotensin type 1 receptor with specific inhibitors candesartan and losartan. Conclusions:The results indicate that angiotensin II modulates cell behaviour via AT1-R and stimulates secretion of MMP-2 by human mammary epithelial cells.

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“…Expression of AT1R has been detected in a variety of tumors, and is associated with a poor prognosis (Ino et al, 2006;Arrieta et al, 2008;De Ronde et al, 2013). Moreover, previous literature has shown that Ang II can modulate tumor cell migration and invasion (Luo et al, 2011;Dominska et al, 2012). Likewise, AT1R blockers (ARBs) can efficiently reduce tumor growth, angiogenesis, and metastasis in mouse experimental models (Deshayes and Nahmias, 2005;George et al, 2010;Wasa et al, 2011).…”

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confidence: 99%

Ang II-AT1R Increases Cell Migration Through PI3K/AKT and NF-κB Pathways in Breast Cancer

Zhao

Wang

et al. 2014

J. Cell. Physiol

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Angiotensin II (Ang II), a biologically active peptide of the renin-angiotensin system (RAS), plays an important role in promoting cell migration via Angiotensin II type 1 receptor (AT1R). In this study, we examined the mechanisms by which Ang II affected cell migration in AT1R-positive MDA-MB-231 human breast cancer cells. Ang II increased cell migration and expression of matrix metalloproteinase (MMP)-2,-9 in a dose-dependent manner. Ang II-mediated cell migration was reduced by specific blocking of MMP-2 and MMP-9, as well as with pretreatment with inhibitors of AT1R, phosphatidylinositol 3-kinase (PI3K), Akt, and NF-κB. Similarly, Ang II-mediated expression of MMP-2,-9 was downregulated by pretreatment with inhibitors of AT1R and PI3K. In addition, Ang II treatment significantly induced phosphorylation of PI3K, Akt, and resulted in increased NF-κB activity. These findings suggest that Ang II activates the AT1R/PI3K/Akt pathway, which further activates IKKα/β and NF-κB, resulting in enhanced expression of MMP-2,-9 and migration in human breast cancer cells. Therefore, targeting Ang II/AT1R/PI3K/Akt/NF-κB signaling could be a novel anti-metastatic therapy for breast cancer.

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Similarities and differences between effects of angiotensin III and angiotensin II on human prostate cancer cell migration and proliferation

Cited by 25 publications

References 28 publications

Interaction between angiotensin II and relaxin 2 in the progress of growth and spread of prostate cancer cells

Interaction between angiotensin II and relaxin 2 in the progress of growth and spread of prostate cancer cells

Angiotensin modulates human mammary epithelial cell motility

Ang II-AT1R Increases Cell Migration Through PI3K/AKT and NF-κB Pathways in Breast Cancer

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