Modulation of metalloproteinase-9 in U87MG glioblastoma cells by A3 adenosine receptors

The A3Adenosine Receptor: History and Perspectives

“…This pathway was also observed in cardiac myocytes subjected to ischemia/hypoxia and reperfusion/reoxygenation (Hussain et al, 2014). In human melanoma A375 and glioblastoma cells, A 3 AR stimulation has produced PI3K-dependent phosphorylation of Akt with antiproliferative effect and MMP-9 increase, respectively (Merighi et al, 2005b;Gessi et al, 2010b).…”

“…In contrast, The A 3 Receptor: History and Perspectives some studies showed that A 3 AR agonist inhibition of cell proliferation was only obtained by micromolar concentrations (Lu et al, 2003;Merighi et al, 2005b;Nakamura et al, 2006). Furthermore, in U87MG cells, A 3 AR stimulation induced an increase in MMP-9, through the AP-1 activation responsible for increased glioblastoma cell invasion, as observed in macrophages (Velot et al, 2008;Gessi et al, 2010b). However, other studies reported that A 3 ARs reduces the ability of prostate cancer cells to migrate in vitro and metastasize in vivo (Jajoo et al, 2009).…”

“…In particular, A 3 ARs are present in different types of tumor cells, such as HL60 and K562 human leukemia , Jurkat , and U937 human lymphoma (Gessi et al, 2010a), Nb2 rat lymphoma (Fishman et al, 2000), A375 human melanoma , PGT-beta mouse tumor pineal gland (Suh et al, 2001), human glioblastoma (Merighi et al, 2006;Gessi et al, 2010b), human prostatic (Jajoo et al, 2009), and mesothelioma cells . A 3 AR subtype overexpression has also been demonstrated in colon cancer tissues, compared with normal mucosa, obtained from patients undergoing surgery (Gessi et al, 2004a;Madi et al, 2004).…”

Purinergic signalling and cancer

“…Adenosine modulates VEGF expression via hypoxia-inducible factor-1 in human hypoxic U87MG and A172 glioblastoma cells via A 3 receptors [629]. Modulation of metalloproteinase-9 in U87MG cells via A 3 receptors has been reported [630]. Pulsed electromagnetic field exposure significantly increased the anti-tumour effect mediated by A 3 receptors in a human glioblastoma cell line [631].…”

BAFF and APRIL induce inflammatory activation of THP-1 cells through interaction with their conventional receptors and activation of MAPK and NF-κB

“…The expression of MMP-2 was not increased by stimulation, as its expression levels are independent of the activation status of macrophages. MMPs (proMMPs) are secreted from the cells as inactive zymogens and then cleaved into active form by protease [25,26]. Treatment with mAbs against the receptors resulted in the expression of the precursor form of both MMP-9 and MMP-2, and conversion of them into the active form was not detected.…”