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

Department of Comparative Endocrinology, Medical University of Lodz, Poland. Electronic address: .
Peptides (Impact Factor: 2.62). 08/2012; 37(2):200-6. DOI: 10.1016/j.peptides.2012.07.022
Source: PubMed


Proliferation plays a critical role in tumor growth when cell migration is essential to invasion. The effect of Ang III and Ang II was evaluated on these important processes. Changes in the migration potential of prostate cancer cells were investigated using Wound Healing Test and a Transwell Migration Chamber with a 3μm pore size. Cell proliferation was measured with a BrdU Assay and Countess Automated Cell Counter, thus determining the influence of angiotensins on hormone-dependent (LNCaP) and hormone-independent (DU-145) human prostate cancer lines. The influence of Ang III and Ang II on classic receptors may be inhibited by Losartan or PD123319. Test peptide modulation of the AT1 and AT2 receptors was examined by Western Blot and fluorescent immunocytochemistry. The results indicate that Ang III promotes the migration of both LNCaP and DU-145 lines, whereas Ang II stimulates this process only in androgen-independent cells. Both angiotensin peptides can induce prostate cancer cell proliferation in a time- and dose-dependent manner. The obtained results show that Ang III and Ang II can modify the expression of classic receptors, particularly AT2. These results suggest that the investigated peptide can modulate cell migration and proliferation in prostate cancer cells. Angiotensins probably have a greater influence on proliferation in the early-stage prostate cancer model than hormone-independent cell lines. Assume also that Ang II can enhance the migration tendency aggressive prostate cancer cells, while Ang III does so more effective in non-metastatic cells.

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Available from: Agnieszka Wanda Piastowska-Ciesielska, Jan 02, 2015
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    • "Ang II exerts major regulatory actions via activation of the Gq/11 protein-coupled angiotensin II receptor type 1 (AT1-R) [9, 15]. In many tissues (including the prostate), activation of the AT1 receptor leads to cell growth and differentiation responses through downstream signalling molecules that include phospholipase C, protein kinase C (PKC), the Ras-Raf-MEK-ERK signalling pathway, and signal transducers and activators of transcription (STATs) [15, 16]. "
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