Angiotensin II stimulation of Na+/K+ATPase activity and cell growth by calcium-independent pathway in MCF-7 breast cancer cells

Muscella, Antonella; Greco, Simona; Elia, Maria Giovanna; Storelli, Carlo; Marsigliante, Santo

doi:10.1677/joe.0.1730315

Cited by 95 publications

(84 citation statements)

References 50 publications

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“…It has been reported that AT 1 R is involved in the proliferation of various cancers in vitro and in vivo (Fujimoto et al, 2001;Rivera et al, 2001;Muscella et al, 2002;Ino et al, 2003;Uemura et al, 2003). However, our immunohistochemical study showed that the AT 1 R expression score did not significantly correlate with the positivity of the cellular proliferation marker PCNA in ovarian cancer tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin II also acts as a potent growth factor not only for vascular smooth muscle cells, but also for certain cancer cell lines (Fujimoto et al, 2001;Muscella et al, 2002). In addition, angiotensin II stimulates angiogenesis via the upregulation of vascular endothelial growth factor (VEGF) (Le Noble et al, 1993;Chua et al, 1998;Pupilli et al, 1999;Tamarat et al, 2002).…”

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confidence: 99%

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Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

et al. 2006

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Angiotensin II, a main effector peptide in the renin -angiotensin system, acts as a growth-promoting and angiogenic factor via type 1 angiotensin II receptors (AT 1 R). We have recently demonstrated that angiotensin II enhanced tumour cell invasion and vascular endothelial growth factor (VEGF) secretion via AT 1 R in ovarian cancer cell lines in vitro. The aim of the present study was to determine whether AT 1 R expression in ovarian cancer is correlated with clinicopathological parameters, angiogenic factors and patient survival. Immunohistochemical staining for AT 1 R, VEGF, CD34 and proliferating cell nuclear antigen (PCNA) were analysed in ovarian cancer tissues (n ¼ 67). Intratumour microvessel density (MVD) was analysed by counting the CD34-positive endothelial cells. Type 1 angiotensin II receptors were expressed in 85% of the cases examined, of which 55% were strongly positive. Type 1 angiotensin II receptors expression was positively correlated with VEGF expression intensity and MVD, but not with histological subtype, grade, FIGO stage or PCNA labelling index. In patients who had positive staining for AT 1 R, the overall survival and progression-free survival were significantly poor (P ¼ 0.041 and 0.017, respectively) as compared to those in patients who had negative staining for AT 1 R, although VEGF, but not AT 1 R, was an independent prognostic factor on multivariate analysis. These results demonstrated that AT 1 R correlated with tumour angiogenesis and poor patient outcome in ovarian cancer, suggesting its clinical potential for a novel molecular target in strategies for ovarian cancer treatment.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

et al. 2006

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“…c-fos is induced by all studied (co)mitogenic stimuli, including TSH (cAMP), insulin/ insulin-like growth factor-I, phorbol esters, serum and growth factors in FRTL-5 (Colletta et al 1986, Isozaki & Kohn 1987, and Wistar rat thyroid (WRT) cells (Tominaga et al 1994), and in dog (Deleu et al 1999) and human thyrocytes (Huber et al 1991, Heinrich & Kraiem 1997. c-fos expression has been claimed to be required for TSHdependent proliferation of Fisher rat thyroid low serum (FRTL)-5 cells (Foti et al 1990), and the activation of AT1 receptors has been shown to induce, in other cell systems, the expression of c-fos (Muscella et al 2002).…”

Section: Discussionmentioning

confidence: 99%

“…The conversion of MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenol tetrazolium bromide) by PC Cl3 cells was used as an indicator of cell number as described by Mosmann (1983), with some modification as described previously (Muscella et al 2002). This method measures the reduction of MTT by active mitochondria, which results in a colorimetric change measured at optical density 570.…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Angiotensin II does not stimulate proliferation of rat thyroid PC Cl3 cell line

Romano¹,

Muscella²,

Storelli³

et al. 2006

Journal of Endocrinology

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In PC Cl3 cells, a rat thyroid cell line, angiotensin (Ang II) activates the atypical protein kinase C-z (PKC-z) and the extracellular signal-regulated kinase (ERK) pathways. We here studied the Ang II effects on PC Cl3 cell proliferation. It was found that Ang II: (1) induced the phosphorylation of protein kinase B (PKB), (2) induced the growth-related early gene c-fos expression, (3) enhanced the cyclin E and p27 kip expression, (4) had no effects on Cdk2, and (5) did not affect the transition from G0/G1 to S phase. Inhibition of phosphoinositide-3kinase by LY294002 further increased the effect of Ang II on p27 kip induction, whilst PKCs inhibition by GF109203X decreased such effect. The role of PKC-z was recognized by the use of a synthetic myristoylated peptide with sequences based on the endogenous PKC-z pseudosubstrate and by PKC-z downregulation using the small interfering RNA (siRNA). Insulin had a replicating effect on PC Cl3 cells, induced the phosphorylation of PKB, decreased p27 kip expression and had no effect on the PKC-z cytosol-to-membrane translocation. PC Cl3 cell proliferation was induced more potently by simultaneous stimulation with insulin and Ang II than by stimulation with insulin alone, and the effect on p27 kip expression was similar to that obtained with insulin only. These observations demonstrate that in PC Cl3 cells Ang II causes a block in G1 phase, although both ERK and PKB pathways are activated, and this effect may be due to the upregulation of p27 kip and PKC-z operativity.

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“…The conversion of 3-(4.5-dimethylthiazol-2-yl)-2.5-diphenol tetrazolium bromide (MTT) by cells was used as an indicator of cell numbers as previously described (30). This method measured the reduction of MTT by active mitochondria, which resulted in a colour change measured at a 550-nm wavelength.…”

Section: Real-time Quantitative Pcr (Rti-qpcr) and Northern Blot Analmentioning

confidence: 99%

miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors

Marsigliante

2012

Int J Oncol

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Abstract. An altered expression of microRNAs (miRNAs) contributes both to the development of cancer and to the progression of the disease. Malignant tumours and tumour cell lines have widespread deregulated expressions of miRNAs compared to normal tissues. In this study, we investigated the expression profiles of 340 mammalian miRNAs in 93 cases of multiform glioblastoma (primary and secondary glioblastoma tumours), by means of DNA microarrays. We show that the expression profiles of 10 miRNAs can distinguish primary from secondary glioblastoma types. Moreover, we found elevated miR-155 levels in primary and secondary glioblastoma tissues as well as in glioblastoma primary cultures. We hypothesised that γ-aminobutyric acid A receptor 1 (GABRA1) is a miR-155 target, and studied the correlation between miR-155 up-regulation and the GABRA1 protein in cultured glioblastoma cells by miRNA silencing. We show that a decrease in miR-155 expression to normal levels restores the expression of GABRA1, making glioblastoma cells sensitive to signals that inhibit cell proliferation mediated by GABRA1. In conclusion, the expression patterns of different miRNAs characterise primary and secondary glioblastomas. The aberrant overexpression of miR-155 contributes to the malignant phenotype of glioblastoma cells removing growth inhibition.

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Angiotensin II stimulation of Na+/K+ATPase activity and cell growth by calcium-independent pathway in MCF-7 breast cancer cells

Cited by 95 publications

References 50 publications

Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

Angiotensin II does not stimulate proliferation of rat thyroid PC Cl3 cell line

miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors

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