1337: Inhibitory Effect of Tamsulosin on Normal Human Prostate Epithelial and Stromal Cells

Transforming growth factor-β1 (TGF-β1) is implicated in prostate development, and elevated expression of TGF-β1 has been correlated with prostate carcinogenesis. In this study, cell type specificity of TGF-β1 and TGF-β receptor Type II (RcII) protein expression was determined by immunocytochemistry in human normal prostate and compared to prostate carcinoma tissues. Heterogeneous localization patterns of LAP-TGF-β1 (TGF-β1 precursor) and RcII were observed in both epithelial and mesenchymal cells in fetal prostate, with LAP-TGF-β1 localizing to more basal epithelial cells. Homogeneity of LAP-TGF-β1 staining was increased in neonatal, prepubertal, and adult prostate, with elevated immunoreac-tivity noted in epithelial acini relative to stromal tissue for both LAP-TGF-β1 and RcII proteins. In stromal tissues, RcII cell localization exhibited staining patterns nearly identical to smooth muscle α-actin. In prostate carcinoma, LAP-TGF-β1 localized to carcinoma cells with an increased staining heterogeneity relative to normal prostate. In contrast to normal epithelial cells, carcinoma epithelial cells exhibited low to nondetectable RcII staining. Stromal cell staining patterns for LAP-TGF-β1 and RcII in carcinoma, however, were identical to those of normal prostate stromal cells. These studies implicate both epithelial and stromal cells as sites of TGF-β1 synthesis and RcII localization in the developing and adult normal human prostate. In addition, these data indicate a loss of epithelial expression of RcII concurrent with altered LAP-TGF-β1 expression in human prostate carcinoma cells.

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Differential effects of vitamin D on normal human prostate epithelial and stromal cells in primary culture

Urology ◽

10.1016/s0090-4295(99)00103-x ◽

1999 ◽

Vol 54 (1) ◽

pp. 171-177 ◽

Cited By ~ 27

Author(s):

D Krill ◽

J Stoner ◽

B.R Konety ◽

M.J Becich ◽

R.H Getzenberg

Keyword(s):

Vitamin D ◽

Primary Culture ◽

Stromal Cells ◽

Human Prostate ◽

Differential Effects ◽

Normal Human

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Transactivation of ErbB1 and ErbB2 receptors by angiotensin II in normal human prostate stromal cells

The Prostate ◽

10.1002/pros.10160 ◽

2002 ◽

Vol 54 (1) ◽

pp. 1-7 ◽

Cited By ~ 28

Author(s):

Jianqing Lin ◽

Michael R. Freeman

Keyword(s):

Angiotensin Ii ◽

Stromal Cells ◽

Human Prostate ◽

Normal Human

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The Nature of the Inhibitory Effect of Normal Human Gastric Jiuice on Heidenhain Pouch Dogs

Gastroenterology ◽

10.1016/s0016-5085(58)80100-6 ◽

1958 ◽

Vol 34 (2) ◽

pp. 181-187 ◽

Cited By ~ 21

Author(s):

William O. Smith ◽

Robert Hoke ◽

Jerome Landy ◽

Ranwel Caputto ◽

Stewart Wolf

Keyword(s):

Inhibitory Effect ◽

Heidenhain Pouch ◽

Normal Human

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667: Sonic Hedgehog Signaling Plays a Pivotal Role in the Vicious Cycle between Human Prostate Cancer and Normal/Benign but not Cancer Associated Human Prostate Stromal Cells

The Journal of Urology ◽

10.1016/s0022-5347(18)30907-8 ◽

2007 ◽

Vol 177 (4S) ◽

pp. 224-224

Author(s):

Katsumi Shigemura ◽

Wen-Chin Haung ◽

Fray F. Marshall ◽

Haiyen E. Zhau ◽

Leland W.K. Chung ◽

...

Keyword(s):

Prostate Cancer ◽

Sonic Hedgehog ◽

Stromal Cells ◽

Hedgehog Signaling ◽

Pivotal Role ◽

Human Prostate ◽

Human Prostate Cancer ◽

Vicious Cycle ◽

Sonic Hedgehog Signaling

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Inhibition of the Activities of α2-Plasmin inhibitor (PI) and CI inhibitor (CI-Inh) by the Synthetic Fibrinolytic Agent, 3-Hydroxypropyl Flufenamide (Flu-HPA)

10.1055/s-0038-1665785 ◽

1979 ◽

Author(s):

L Miles ◽

J Burnier ◽

M Verlander ◽

M Goodman ◽

A Kleiss ◽

...

Keyword(s):

Plasminogen Activators ◽

Inhibitory Effect ◽

Mechanisms Of Action ◽

Flufenamic Acid ◽

Clot Lysis ◽

Factor Xiia ◽

Dependent Inhibition ◽

Normal Human ◽

Plasmin Inhibitor

Flu-HPA is one of a series of flufenamic acid derivations that enhances plasminogen-dependent clot lysis in vitro. Studies of possible mechanisms of action of Flu-HPA were undertaken. The influence of Flu-HPA on the inhibition of purified plasmin by purified PI was studied. PI activity was assessed by its inhibition of the clevage of the tripeptide S-2251 (H-D-Val-Leu-Lys-pNA) by plasmin. Flu-HPA was dissolved in DMF or in methonol and preincubated with PI before addition of plasmin. At Flu-HPA concentrations greater than 1mM and up to 60mM, the inhibitory activity of PI was totally lost. The inhibitory effect of normal human plasma on plasmin was also completely abolished at concentrations of Flu-HPA between 2.5 and 40mM. The effect of Flu-HPA on the inhibition of purified plasma kallikrein by purified CI-Inh was also studied. CI-Inh activity was measured by its inhibition of cleavage of the tripeptide Bz-Pro-Phe-Arg-pNA by kallikrein. When Flu-HPA, dissolved in DMF or in methonol, was preincubated with CI-Inh, a concentration dependent inhibition of CI-Inh activity was observed. CI-Inh activity was abolished by concentrations of Flu-HPA greater than 1mM. Flu-HPA also inhibited the activity of CI-Inh on purified Factor XIIa. These observations suggest that this flufenamic acid derivative may enhance fibrinolysis not only by inhibiting PI activity but also by decreasing the inactivation of plasminogen activators by CI-Inh.

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ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

Acta Endocrinologica ◽

10.1530/acta.0.0740263 ◽

1973 ◽

Vol 74 (2) ◽

pp. 263-270 ◽

Cited By ~ 50

Author(s):

Yoshikatsu Nakai ◽

Hiroo Imura ◽

Teruya Yoshimi ◽

Shigeru Matsukura

Keyword(s):

Intravenous Infusion ◽

Human Subjects ◽

Blocking Agent ◽

Inhibitory Effect ◽

Plasma Acth ◽

Acth Secretion ◽

Glucose Levels ◽

Alpha Receptors ◽

Normal Human ◽

Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

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INHIBITION BY HUMAN SERUM OF THE ADIPOKINETIC EFFECT OF A HUMAN PITUITARY LIPID-MOBILIZING FACTOR

Acta Endocrinologica ◽

10.1530/acta.0.0710443 ◽

1972 ◽

Vol 71 (3) ◽

pp. 443-453 ◽

Cited By ~ 2

Author(s):

Olav Trygstad ◽

Irene Foss

Keyword(s):

Human Serum ◽

Gel Filtration ◽

Deae Cellulose ◽

Inhibitory Effect ◽

Disc Electrophoresis ◽

Inhibitory Protein ◽

Human Pituitary ◽

Albumin Fraction ◽

Pituitary Glands ◽

Normal Human

ABSTRACT A lipid-mobilizing factor (LMF) with an adipotrophic effect in human and animal fat tissue has been prepared from human pituitary glands. The addition of normal human serum to LMF reduced its lipolytic effect, and it was completely abolished by serum from a group of obese patients, whereas the lipolysis was not influenced by serum from patients with generalized lipodystrophy. By DEAE-cellulose chromatography of human serum the inhibitory effect on LMF was found to be present in a protein fraction less acidic than the main serum albumin fraction. The inhibitory fraction was deprived of some contaminants by Sephadex gel filtration. Disc electrophoresis demonstrated the presence of three components in the inhibitory protein (IP), and they were identified as albumin, transferin, and haemopexin by immuno-electrophoresis. Precipitation of these proteins by their rabbit antisera demonstrated that the inhibitory effect was present in the albumin fraction. Insulin like activity was not observed in IP. A protein binding of LMF by IP could not be demonstrated. Incubation at 37°C for one hour of a mixture of LMF and IP eliminated the electrophoretic picture of LMF. It is concluded that the inhibitory effect of human serum may be due to proteolysis of LMF.

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The inhibitory effect of melatonin on human prostate cancer

Cell Communication and Signaling ◽

10.1186/s12964-021-00723-0 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Dexin Shen ◽

Lingao Ju ◽

Fenfang Zhou ◽

Mengxue Yu ◽

Haoli Ma ◽

...

Keyword(s):

Prostate Cancer ◽

Clinical Trials ◽

Theoretical Basis ◽

Inhibitory Effect ◽

Human Prostate ◽

Human Prostate Cancer ◽

Anti Oxidant ◽

Androgen Depletion ◽

The Relationship ◽

Future Utilization

AbstractProstate cancer (PCa) is one of the most commonly diagnosed human cancers in males. Nearly 191,930 new cases and 33,330 new deaths of PCa are estimated in 2020. Androgen and androgen receptor pathways played essential roles in the pathogenesis of PCa. Androgen depletion therapy is the most used therapies for primary PCa patients. However, due to the high relapse and mortality of PCa, developing novel noninvasive therapies have become the focus of research. Melatonin is an indole-like neurohormone mainly produced in the human pineal gland with a prominent anti-oxidant property. The anti-tumor ability of melatonin has been substantially confirmed and several related articles have also reported the inhibitory effect of melatonin on PCa, while reviews of this inhibitory effect of melatonin on PCa in recent 10 years are absent. Therefore, we systematically discuss the relationship between melatonin disruption and the risk of PCa, the mechanism of how melatonin inhibited PCa, and the synergistic benefits of melatonin and other drugs to summarize current understandings about the function of melatonin in suppressing human prostate cancer. We also raise several unsolved issues that need to be resolved to translate currently non-clinical trials of melatonin for clinic use. We hope this literature review could provide a solid theoretical basis for the future utilization of melatonin in preventing, diagnosing and treating human prostate cancer.

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