Abstract
Secretory leukocyte protease inhibitor is a multifunctional protein with a variety of activities attributed to it. A significant increase in the expression of Secretory leukocyte protease inhibitor was noticed in syncytiotrophoblasts following differentiation of cytotrophoblasts in to syncytiotrophoblasts by addition of Forskolin. Using the BeWo cells which are derived from choriocarcinoma, the effect of addition of progesterone and estradiol on the expression of Secretory leukocyte protease inhibitor by Reverse Transcription Polymerase Chain Reaction was assessed. It was found that while addition of low concentration of progesterone resulted in a significant increase in expression of Secretory leukocyte protease inhibitor, addition of estradiol even at high concentration had no effect. The specificity of effect of progesterone was established by the observation that addition of Progesterone along with progesterone receptor antagonist (RU484) resulted in decrease in the level of expression of Secretory leukocyte protease inhibitor. These results suggest that Secretory protease leukocyte protease inhibitor is a progesterone regulated gene.
Highlights
The critical role of androgenic hormones in prostate cancer (PCa) has been well-recognized for almost seventy years, ever since Huggins and Hodges first reported the significant clinical effects of suppressing serum androgen levels in men with advanced PCa in 1941[1]
It is possible that castration resistant PCa (CRPC) may arise as a consequence of selection pressure imposed by ADTs that favours the growth of androgen-insensitive cells [3,4], recent evidence indicates that growth of the vast majority of cancer cells in tumors relapsing from castration still depend heavily on the androgen receptor (AR) signaling axis [5,6,7,8,9,10,11], in an adaptation process called “AR reactivation” that involves a variety of mechanisms
Reports show that administration of finasteride or dutasteride was able to cause ~25% reduction of PCa risk compared with placebos [92,93], at an unfortunate cost to increase the incidence of high-grade prostate cancers
Summary
The critical role of androgenic hormones in prostate cancer (PCa) has been well-recognized for almost seventy years, ever since Huggins and Hodges first reported the significant clinical effects of suppressing serum androgen levels in men with advanced PCa in 1941[1]. It is possible that CRPC may arise as a consequence of selection pressure imposed by ADTs that favours the growth of androgen-insensitive cells [3,4], recent evidence indicates that growth of the vast majority of cancer cells in tumors relapsing from castration still depend heavily on the AR signaling axis [5,6,7,8,9,10,11], in an adaptation process called “AR reactivation” that involves a variety of mechanisms (reviewed in ref [12,13,14]) Based on this understanding, multiple novel AR signaling-targeting reagents for CRPC have been under active trial or development, some of which have shown promising clinical effects (reviewed in ref [13,15,16,17]).
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