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

Abstract

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.

DJ‐1 Alleviates Angiotensin II‐Induced Endothelial Progenitor Cell Damage by Activating the PPARγ/HO‐1 Pathway

“…Ang II can be detected easily in atherosclerotic plaques due to its high level of expression [Hoshida et al, 2001], which can impair the function and accelerate the senescence of EPCs [Zhou et al, 2010]. This is distinct from the growth-promoting effect of Ang II in many types of cancer cells [Dominska et al, 2016;Nowakowska et al, 2016]. Although the diminished effects of Ang II on the migration, adhesion, and tube formation of EPCs can be restored by natural extracts [Parzonko et al, 2013], they are not easily administered.…”

Angiotensin 1–7 modulates molecular and cellular processes central to the pathogenesis of prostate cancer

“…Other researchers have also reported modulation of cell adhesion to the ECM by angiotensins. We observed previously that AngII improved ability of prostate cancer cells to adhere to the ECM 13 . Many other studies have demonstrated that Ang1–7 has an antagonistic effects than Ang II.…”

“…Our results clearly show that Ang1–7 can inhibit the anchorage-independent growth and non-adherent colony formation of both LNCaP and DU-145 cells, but not PC3. In contrast, Ang II was earlier observed to have a statistically insignificant stimulatory effect in all tested prostate cancer cells 13 .…”

“…The transwell migration/invasion assays were performed as described previously 13 . All cell lines were incubated with Ang1–7 (1 nM) on 6-well plates for 48 hours.…”

“…First, the gel was incubated in a developing buffer (0.5 M Tris-HCl, 2 M NaCl, 50 mM CaCl 2 , pH 7.5) and then with Coomassie Brilliant Blue R-250 staining buffer. Following this, a discoloring buffer comprising methanol: acetic acid: water (3: 1: 6) was added to identify clear bands on the dark background, as previously described 13 . The gelatinolytic activity of enzymes in samples was further evaluated based on the band area using ImageJ software.…”