Regulation of progesterone receptor isoforms content in human astrocytoma cell lines

Progesterone receptor and SRC-1 participate in the regulation of VEGF, EGFR and Cyclin D1 expression in human astrocytoma cell lines

“…In astrocytomas, a direct relation between the content of PR and the tumor grade has been reported, suggesting that PR-positive tumors possess a high proliferative potential [8,14]. Our group has found that P induces cell proliferation in U373 and D54 human astrocytoma cell lines (grades III and IV, respectively), which is blocked by its antagonist RU 486, suggesting that P effects are mediated by PR [15] whose both isoforms have been detected in U373 and D54 cells [16,17].It has been demonstrated that the expression of VEGF, EGFR and cyclin D1 directly correlates with the tumor grade and the recurrence of astrocytomas [3,5]. Several studies have established that natural and synthetic progestins increase VEGF, EGFR and cyclin D1 expression (mRNA and protein) in human endothelial, Ishikawa endometrial carcinoma and breast cancer cells (BT-474, T47D and HCC-1428) through a PR-mediated mechanism [18][19][20][21].…”

Progesterone and estradiol effects on SRC-1 and SRC-3 expression in human astrocytoma cell lines

“…In U373 cells, we have recently reported that PR isoforms expression was up-regulated by E 2 and that this effect was blocked by ER antagonist, ICI182780, suggesting that PR regulation by E 2 depends on ER activation [19].…”

Effects of progesterone on the content of CCR5 and CXCR4 coreceptors in PBMCs of seropositive and exposed but uninfected Mexican women to HIV-1

“…Proteins (50 g) were separated by electrophoresis in 10% SDS-PAGE and transferred to nitrocellulose membranes (Amersham, NJ, USA). They were blocked at room temperature with 3% non-fat dry milk and 1% bovine serum albumin for 2 h [21]. Membranes were then incubated overnight with mouse-anti-PR polyclonal antibody (2 g/ml) (NeoMarkers RB-1492-P, Fremont, CA), mouse-anti-CCR5 (1 g/ml) (IgG-HRP CKR5, Santa-Cruz sc-17833) or with rabbit-anti-CXCR4 (5 g/ml) (IgG-HRP CD184, Chemicon AB-1847) at 4 • C. The resulting blots were then incubated with secondary antibody conjugated to horseradish peroxidase (Santa Cruz Biotechnology, Santa Cruz, CA) for 45 min.…”

“…To correct differences in the amount of total protein loaded in each lane, CCR5 and CXCR4 protein contents were normalized to that of ␣-tubulin as previously reported [21]. The intensity of CCR5, CXCR4 and ␣-tubulin signals was quantified by densitometry using Scan Primax 600p apparatus (Colorado, Utrecht, the Netherlands) and the Scion Image software (Scion Corp., Maryland).…”

“…Two main PR isoforms have been reported in humans -the full length form (PR-B, 114 kDa) and the truncated N-terminal form (PR-A, 94 kDa) -with different function and regulation. P effects can be determined by the expression ratio PR-A/PR-B [21][22][23]. In general, PR-B is a much stronger transcriptional activator than PR-A, due to an additional activation function (AF) domain in the amino terminus of PR-B [24].…”