Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients. / Stroomberg, Hein Vincent; Jørgensen, Anne; Brasso, Klaus; Nielsen, John Erik; Juul, Anders; Frederiksen, Hanne; Blomberg Jensen, Martin; Røder, Martin Andreas.

I: PLoS ONE, Bind 15, Nr. 9, e0238814, 2020.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Stroomberg, HV, Jørgensen, A, Brasso, K, Nielsen, JE, Juul, A, Frederiksen, H, Blomberg Jensen, M & Røder, MA 2020, 'Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients', PLoS ONE, bind 15, nr. 9, e0238814. https://doi.org/10.1371/journal.pone.0238814

APA

Stroomberg, H. V., Jørgensen, A., Brasso, K., Nielsen, J. E., Juul, A., Frederiksen, H., Blomberg Jensen, M., & Røder, M. A. (2020). Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients. PLoS ONE, 15(9), [e0238814]. https://doi.org/10.1371/journal.pone.0238814

Vancouver

Stroomberg HV, Jørgensen A, Brasso K, Nielsen JE, Juul A, Frederiksen H o.a. Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients. PLoS ONE. 2020;15(9). e0238814. https://doi.org/10.1371/journal.pone.0238814

Author

Stroomberg, Hein Vincent ; Jørgensen, Anne ; Brasso, Klaus ; Nielsen, John Erik ; Juul, Anders ; Frederiksen, Hanne ; Blomberg Jensen, Martin ; Røder, Martin Andreas. / Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients. I: PLoS ONE. 2020 ; Bind 15, Nr. 9.

Bibtex

@article{0a4eb8bac7ae4cc88647fc5e03069b16,
title = "Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients",
abstract = "Prostate cancer (PCa) cells become castrate-resistant after initial tumor regression following castration-based lowering of testosterone (T). De-novo intra-tumoral steroid synthesis is a suggested biological mechanism of castration resistant PCa, but the regulators are unknown. Testicular T production is controlled by the luteinizing hormone/choriogonadotropin receptor (LHCGR). To elucidate the influence of LHCGR on PCa development the presence and effects of LHCGR in PCa and whether LHCGR in serum holds prognostic information in PCa patients is investigated. LHCGR expression was investigated by RT-PCR, WB, IHC, qPCR in PCa cell lines and prostatic tissue. Steroid production was measured in media from cell lines with LC-MS/MS and expression of steroidogenic enzymes with qPCR. Serum LHCGR (sLHCGR) was measured with ELISA in PCa patients (N = 157). Presence of LHCGR was established in prostatic tissue and PCa cell lines. Cell proliferation increased by 1.29-fold in LNCaP (P = 0.007) and 1.33-fold in PC-3 cells (P = 0.0007), when stimulated by luteinizing hormone. Choriogonadotropin stimulation decreased proliferation 0.93-fold in DU145 cells (P = 0.05), but none of the treatments altered steroid metabolite secretion. Low sLHCGR concentration was associated with a higher risk of biochemical failure after radical prostatectomy (HR = 3.05, P = 0.06) and castration resistance (HR = 6.92, P = 0.004) compared to high sLHCGR concentration. LHCGR is expressed in PCa and may exert a growth regulatory role in PCa derived cell lines. A potential prognostic role of sLHCGR for determining recurrence risk in PCa patients is found in this pilot study but needs verification in larger cohorts.",
keywords = "Aged, Chorionic Gonadotropin/pharmacology, Humans, Luteinization/drug effects, Luteinizing Hormone/metabolism, Male, Middle Aged, Pilot Projects, Prostate/pathology, Prostatectomy/adverse effects, Prostatic Neoplasms/physiopathology, Receptors, LH/metabolism, Testis/metabolism, Testosterone/metabolism, Tumor Cells, Cultured",
author = "Stroomberg, {Hein Vincent} and Anne J{\o}rgensen and Klaus Brasso and Nielsen, {John Erik} and Anders Juul and Hanne Frederiksen and {Blomberg Jensen}, Martin and R{\o}der, {Martin Andreas}",
year = "2020",
doi = "10.1371/journal.pone.0238814",
language = "English",
volume = "15",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "9",

}

RIS

TY - JOUR

T1 - Novel functions of the luteinizing hormone/chorionic gonadotropin receptor in prostate cancer cells and patients

AU - Stroomberg, Hein Vincent

AU - Jørgensen, Anne

AU - Brasso, Klaus

AU - Nielsen, John Erik

AU - Juul, Anders

AU - Frederiksen, Hanne

AU - Blomberg Jensen, Martin

AU - Røder, Martin Andreas

PY - 2020

Y1 - 2020

N2 - Prostate cancer (PCa) cells become castrate-resistant after initial tumor regression following castration-based lowering of testosterone (T). De-novo intra-tumoral steroid synthesis is a suggested biological mechanism of castration resistant PCa, but the regulators are unknown. Testicular T production is controlled by the luteinizing hormone/choriogonadotropin receptor (LHCGR). To elucidate the influence of LHCGR on PCa development the presence and effects of LHCGR in PCa and whether LHCGR in serum holds prognostic information in PCa patients is investigated. LHCGR expression was investigated by RT-PCR, WB, IHC, qPCR in PCa cell lines and prostatic tissue. Steroid production was measured in media from cell lines with LC-MS/MS and expression of steroidogenic enzymes with qPCR. Serum LHCGR (sLHCGR) was measured with ELISA in PCa patients (N = 157). Presence of LHCGR was established in prostatic tissue and PCa cell lines. Cell proliferation increased by 1.29-fold in LNCaP (P = 0.007) and 1.33-fold in PC-3 cells (P = 0.0007), when stimulated by luteinizing hormone. Choriogonadotropin stimulation decreased proliferation 0.93-fold in DU145 cells (P = 0.05), but none of the treatments altered steroid metabolite secretion. Low sLHCGR concentration was associated with a higher risk of biochemical failure after radical prostatectomy (HR = 3.05, P = 0.06) and castration resistance (HR = 6.92, P = 0.004) compared to high sLHCGR concentration. LHCGR is expressed in PCa and may exert a growth regulatory role in PCa derived cell lines. A potential prognostic role of sLHCGR for determining recurrence risk in PCa patients is found in this pilot study but needs verification in larger cohorts.

AB - Prostate cancer (PCa) cells become castrate-resistant after initial tumor regression following castration-based lowering of testosterone (T). De-novo intra-tumoral steroid synthesis is a suggested biological mechanism of castration resistant PCa, but the regulators are unknown. Testicular T production is controlled by the luteinizing hormone/choriogonadotropin receptor (LHCGR). To elucidate the influence of LHCGR on PCa development the presence and effects of LHCGR in PCa and whether LHCGR in serum holds prognostic information in PCa patients is investigated. LHCGR expression was investigated by RT-PCR, WB, IHC, qPCR in PCa cell lines and prostatic tissue. Steroid production was measured in media from cell lines with LC-MS/MS and expression of steroidogenic enzymes with qPCR. Serum LHCGR (sLHCGR) was measured with ELISA in PCa patients (N = 157). Presence of LHCGR was established in prostatic tissue and PCa cell lines. Cell proliferation increased by 1.29-fold in LNCaP (P = 0.007) and 1.33-fold in PC-3 cells (P = 0.0007), when stimulated by luteinizing hormone. Choriogonadotropin stimulation decreased proliferation 0.93-fold in DU145 cells (P = 0.05), but none of the treatments altered steroid metabolite secretion. Low sLHCGR concentration was associated with a higher risk of biochemical failure after radical prostatectomy (HR = 3.05, P = 0.06) and castration resistance (HR = 6.92, P = 0.004) compared to high sLHCGR concentration. LHCGR is expressed in PCa and may exert a growth regulatory role in PCa derived cell lines. A potential prognostic role of sLHCGR for determining recurrence risk in PCa patients is found in this pilot study but needs verification in larger cohorts.

KW - Aged

KW - Chorionic Gonadotropin/pharmacology

KW - Humans

KW - Luteinization/drug effects

KW - Luteinizing Hormone/metabolism

KW - Male

KW - Middle Aged

KW - Pilot Projects

KW - Prostate/pathology

KW - Prostatectomy/adverse effects

KW - Prostatic Neoplasms/physiopathology

KW - Receptors, LH/metabolism

KW - Testis/metabolism

KW - Testosterone/metabolism

KW - Tumor Cells, Cultured

U2 - 10.1371/journal.pone.0238814

DO - 10.1371/journal.pone.0238814

M3 - Journal article

C2 - 32881970

VL - 15

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 9

M1 - e0238814

ER -

ID: 256580305