The emerging role of progesterone receptor membrane component 1 (PGRMC1) in cancer biology

2016 ◽  
Vol 1866 (2) ◽  
pp. 339-349 ◽  
Author(s):  
Michael A. Cahill ◽  
Jalal A. Jazayeri ◽  
Susan M. Catalano ◽  
Shinya Toyokuni ◽  
Zaklina Kovacevic ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Cancer Biology ◽  
Membrane Component ◽  
Receptor Membrane

Regulation and role of Progesterone receptor membrane component 1 (PGRMC1) in endometrial stromal cell decidualization

Placenta ◽  
2019 ◽  
Vol 87 ◽  
pp. 69
Author(s):  
Atuya Tsuru ◽  
Mikihiro Yoshie ◽  
Ryo Yonekawa ◽  
Junya Kojima ◽  
Hirotaka Nishi ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Stromal Cell ◽  
Endometrial Stromal Cell ◽  
Membrane Component ◽  
Receptor Membrane

scholarly journals Progesterone Increases the Release of Brain-Derived Neurotrophic Factor from Glia via Progesterone Receptor Membrane Component 1 (Pgrmc1)-Dependent ERK5 Signaling

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4389-4400 ◽  
Author(s):  
Chang Su ◽  
Rebecca L. Cunningham ◽  
Nataliya Rybalchenko ◽  
Meharvan Singh
Keyword(s):  
Progesterone Receptor ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Experimental Models ◽  
Protective Effects ◽  
Membrane Component ◽  
Signaling Mechanism ◽  
Receptor Membrane ◽  
Bdnf Signaling

Progesterone (P4) is cytoprotective in various experimental models, but our understanding of the mechanisms involved is still incomplete. Our laboratory has implicated brain-derived neurotrophic factor (BDNF) signaling as an important mediator of P4's protective actions. We have shown that P4 increases the expression of BDNF, an effect mediated by the classical P4 receptor (PR), and that the protective effects of P4 were abolished using inhibitors of Trk receptor signaling. In an effort to extend our understanding of the interrelationship between P4 and BDNF signaling, we determined whether P4 influenced BDNF release and examined the role of the classical PR and a putative membrane PR, progesterone receptor membrane component-1 (Pgrmc1), as mediators of this response. Given recent data from our laboratory that supported the role of ERK5 in BDNF release, we also tested whether P4-induced BDNF release was mediated by ERK5. In this study, we found that P4 and the membrane-impermeable P4 (P4-BSA) both induced BDNF release from cultured C6 glial cells and primary astrocytes. Both these cells lack the classical nuclear/intracellular PR but express high levels of membrane-associated PR, including Pgrmc1. Using RNA interference-mediated knockdown of Pgrmc1 expression, we determined that P4-induced BDNF release was dependent on the expression of Pgrmc1, although pharmacological inhibition of the PR failed to alter the effects of P4. Furthermore, the BDNF release elicited by P4 was mediated by ERK5, and not ERK1/2. Collectively, our data describe that P4 elicits an increase in BDNF release from glia via a Pgrmc1-induced ERK5 signaling mechanism and identify Pgrmc1 as a potential therapeutic target for future hormone-based drug development for the treatment of such degenerative diseases as Alzheimer's disease as well as other diseases wherein neurotrophin dysregulation is noted.

scholarly journals PGRMC Proteins Are Coming of Age: A Special Issue on the Role of PGRMC1 and PGRMC2 in Metabolism and Cancer Biology

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 512
Author(s):  
Michael A. Cahill ◽  
Hans Neubauer
Keyword(s):  
Cancer Biology ◽  
Coming Of Age ◽  
Special Issue ◽  
Membrane Component ◽  
Receptor Membrane

This is a preface by the guest editors of the special issue of Cancers featuring the biology of progesterone (P4) receptor membrane component (PGRMC) proteins as it relates to metabolism and cancer [...]

Role of Progesterone Receptor Membrane Component-1 (PGRMC-1) on Bovine Oocyte Maturation.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 278-278
Author(s):  
Alberto M. Luciano ◽  
Valentina Lodde ◽  
Federica Franciosi ◽  
Fabrizio Ceciliani ◽  
John J. Peluso
Keyword(s):  
Progesterone Receptor ◽  
Oocyte Maturation ◽  
Bovine Oocyte ◽  
Membrane Component ◽  
Receptor Membrane

scholarly journals Progesterone increases blood glucose via hepatic progesterone receptor membrane component 1 under limited or impaired action of insulin

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Sang R. Lee ◽  
Woo-Young Choi ◽  
Jun H. Heo ◽  
Jiyoung Huh ◽  
Globinna Kim ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Cyclic Amp ◽  
Progesterone Receptor ◽  
Insulin Action ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Membrane Component ◽  
Receptor Membrane ◽  
Hep3b Cells

Abstract Hepatic gluconeogenesis is the main pathway for blood glucose maintenance activated during fasting. Retardation of insulin action, such as in diabetes mellitus, activates gluconeogenesis during the fed state. While the role of progesterone (P4) in diabetes is controversial, the P4 receptor, progesterone receptor membrane component 1 (PGRMC1), is known to stimulate pancreatic insulin secretion. We investigated the role of P4, via hepatic PGRMC1, during gluconeogenesis. The PGRMC1 binding chemical, AG-205, induced PGRMC1 monomer (25 kDa) abundance, and increased PEPCK expression and glucose production in parallel with cyclic AMP (cAMP) induction in Hep3B cells. PGRMC1-mediated cyclic AMP was inhibited by an adenylate cyclase inhibitor (MDL-12,330A). PEPCK suppression in Pgrmc1 KO hepatocyte was not observed after treatment of MDL-12,330A. PGRMC1 knockdown or overexpression systems in Hep3B cells confirmed that PGRMC1 mediates PEPCK expression via phosphorylation of cAMP-response element binding protein (CREB). CREB phosphorylation and PEPCK expression in primary hepatocytes were greater than that in PGRMC1 knock-out hepatocytes. Progesterone increased PGRMC1 expression, which induced cAMP and PEPCK induction and glucose production. In vivo, P4 suppressed gluconeogenesis following plasma insulin induction under normal conditions in a mouse model. However, P4 increased blood glucose via gluconeogenesis in parallel with increases in PGRMC1 and PEPCK expression in mice in both insulin-deficient and insulin-resistant conditions. We conclude that P4 increases hepatic glucose production via PGRMC1, which may exacerbate hyperglycaemia in diabetes where insulin action is limited.

scholarly journals Glycyrrhizin Derivatives Suppress Cancer Chemoresistance by Inhibiting Progesterone Receptor Membrane Component 1

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3265
Author(s):  
Yasuaki Kabe ◽  
Ikko Koike ◽  
Tatsuya Yamamoto ◽  
Miwa Hirai ◽  
Ayaka Kanai ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Cancer Progression ◽  
Egf Receptor ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Human Colon ◽  
Titration Calorimetry ◽  
Membrane Component ◽  
Human Colon Cancer ◽  
Receptor Membrane

Progesterone receptor membrane component 1 (PGRMC1) is highly expressed in various cancer cells and contributes to tumor progression. We have previously shown that PGRMC1 forms a unique heme-stacking functional dimer to enhance EGF receptor (EGFR) activity required for cancer proliferation and chemoresistance, and the dimer dissociates by carbon monoxide to attenuate its biological actions. Here, we determined that glycyrrhizin (GL), which is conventionally used to ameliorate inflammation, specifically binds to heme-dimerized PGRMC1. Binding analyses using isothermal titration calorimetry revealed that some GL derivatives, including its glucoside-derivative (GlucoGL), bind to PGRMC1 potently, whereas its aglycone, glycyrrhetinic acid (GA), does not bind. GL and GlucoGL inhibit the interaction between PGRMC1 and EGFR, thereby suppressing EGFR-mediated signaling required for cancer progression. GL and GlucoGL significantly enhanced EGFR inhibitor erlotinib- or cisplatin (CDDP)-induced cell death in human colon cancer HCT116 cells. In addition, GL derivatives suppressed the intracellular uptake of low-density lipoprotein (LDL) by inhibiting the interaction between PGRMC1 and the LDL receptor (LDLR). Effects on other pathways cannot be excluded. Treatment with GlucoGL and CDDP significantly suppressed tumor growth following xenograft transplantation in mice. Collectively, this study indicates that GL derivatives are novel inhibitors of PGRMC1 that suppress cancer progression, and our findings provide new insights for cancer treatment.

Progesterone receptor membrane component 1 (PGRMC1) expression in canine mammary tumors: A preliminary study

2020 ◽  
Vol 132 ◽  
pp. 101-107
Author(s):  
Laura Terzaghi ◽  
Barbara Banco ◽  
Debora Groppetti ◽  
Priscila C. Dall'Acqua ◽  
Chiara Giudice ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Mammary Tumors ◽  
Membrane Component ◽  
Canine Mammary Tumors ◽  
Receptor Membrane ◽  
Preliminary Study
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