Oxytocin in the tumor microenvironment is associated with lower inflammation and longer survival in advanced epithelial ovarian cancer patients.


Journal

Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148

Informations de publication

Date de publication:
08 2019
Historique:
received: 23 01 2019
revised: 21 03 2019
accepted: 05 04 2019
pubmed: 21 4 2019
medline: 1 4 2020
entrez: 21 4 2019
Statut: ppublish

Résumé

Prior research demonstrates a protective role for oxytocin in ovarian cancer based on its anti-proliferative, anti-migratory, and anti-invasive effects in vitro and in vivo. However, the role of endogenous oxytocin has not been examined in ovarian cancer patients. Oxytocin also has anti-inflammatory properties that have not been examined in cancer. The purpose of this investigation was to examine relationships between endogenous oxytocin, tumor-associated inflammation (interleukin-6), and survival in advanced epithelial ovarian cancer patients. Tumor microenvironment (ascites) and plasma oxytocin levels were analyzed via ELISA on extracted samples obtained from 79 patients. In vitro models were used to characterize oxytocin and oxytocin receptor expression in four ovarian cancer cell lines and to investigate direct anti-inflammatory effects of oxytocin on tumor cell secretion of interleukin-6. High and variable levels of oxytocin were observed in ascites, up to 200 times greater than in plasma. Higher levels of ascites oxytocin were associated with lower levels of systemic and tumor-associated interleukin-6, an inflammatory cytokine implicated in ovarian tumor progression. Oxytocin also attenuated interleukin-6 secretion from multiple ovarian tumor cell lines in vitro. Higher levels of ascites oxytocin were associated with a significant survival advantage and statistical mediation analyses suggested this effect was partially mediated by interleukin-6. These data identify a previously unacknowledged hormone in the ovarian tumor microenvironment and provide initial evidence that oxytocin has protective effects in ovarian cancer via anti-inflammatory mechanisms. Future studies should examine the therapeutic utility of oxytocin.

Sections du résumé

BACKGROUND
Prior research demonstrates a protective role for oxytocin in ovarian cancer based on its anti-proliferative, anti-migratory, and anti-invasive effects in vitro and in vivo. However, the role of endogenous oxytocin has not been examined in ovarian cancer patients. Oxytocin also has anti-inflammatory properties that have not been examined in cancer. The purpose of this investigation was to examine relationships between endogenous oxytocin, tumor-associated inflammation (interleukin-6), and survival in advanced epithelial ovarian cancer patients.
METHODS
Tumor microenvironment (ascites) and plasma oxytocin levels were analyzed via ELISA on extracted samples obtained from 79 patients. In vitro models were used to characterize oxytocin and oxytocin receptor expression in four ovarian cancer cell lines and to investigate direct anti-inflammatory effects of oxytocin on tumor cell secretion of interleukin-6. High and variable levels of oxytocin were observed in ascites, up to 200 times greater than in plasma. Higher levels of ascites oxytocin were associated with lower levels of systemic and tumor-associated interleukin-6, an inflammatory cytokine implicated in ovarian tumor progression. Oxytocin also attenuated interleukin-6 secretion from multiple ovarian tumor cell lines in vitro. Higher levels of ascites oxytocin were associated with a significant survival advantage and statistical mediation analyses suggested this effect was partially mediated by interleukin-6.
CONCLUSIONS
These data identify a previously unacknowledged hormone in the ovarian tumor microenvironment and provide initial evidence that oxytocin has protective effects in ovarian cancer via anti-inflammatory mechanisms. Future studies should examine the therapeutic utility of oxytocin.

Identifiants

pubmed: 31005045
pii: S0306-4530(19)30064-2
doi: 10.1016/j.psyneuen.2019.04.007
pmc: PMC6716948
mid: NIHMS1527306
pii:
doi:

Substances chimiques

Interleukin-6 0
Receptors, Oxytocin 0
Oxytocin 50-56-6

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

244-251

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL116387
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA140933
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA086862
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM108540
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA109298
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA209904
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA193249
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG017265
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG043404
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

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Auteurs

Michaela G Cuneo (MG)

Department of Psychological & Brain Sciences, University of Iowa, United States.

Angela Szeto (A)

Department of Psychology, University of Miami, United States.

Andrew Schrepf (A)

Department of Anesthesiology and Chronic Pain and Fatigue Research Center, University of Michigan, United States.

Ellen M Kinner (EM)

Department of Psychological & Brain Sciences, University of Iowa, United States.

Benjamin I Schachner (BI)

Diabetes Research Institute, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, United States.

Raisa Ahmed (R)

Diabetes Research Institute, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, United States.

Premal H Thaker (PH)

Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Washington University School of Medicine, United States.

Michael Goodheart (M)

Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Iowa, United States; Holden Comprehensive Cancer Center, University of Iowa, United States.

David Bender (D)

Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Iowa, United States.

Steve W Cole (SW)

Department of Medicine, Division of Hematology/Oncology and Molecular Biology Institute, David Geffen School of Medicine, University of California, Los Angeles, United States.

Philip M McCabe (PM)

Department of Psychology, University of Miami, United States.

Anil K Sood (AK)

Departments of Gynecologic Oncology, Cancer Biology and Center for RNA Interference and Noncoding RNA, University of Texas M.D. Anderson Cancer Center, United States.

Susan K Lutgendorf (SK)

Department of Psychological & Brain Sciences, University of Iowa, United States; Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Iowa, United States; Holden Comprehensive Cancer Center, University of Iowa, United States. Electronic address: susan-lutgendorf@uiowa.edu.

Armando J Mendez (AJ)

Diabetes Research Institute, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, United States.

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Classifications MeSH