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The intricate hormonal interplay essential for male reproductive health begins with the release of gonadotropin-releasing hormone (GnRH) by the hypothalamus. This hormone prompts the pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH targets the Leydig cells in the testes, stimulating them to produce and release testosterone. In concert with testosterone, FSH acts on the Sertoli cells within the seminiferous tubules to facilitate the release of...
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The ovarian cycle regulates endometrial changes throughout a single menstrual cycle via the coordinated action of gonadotrophin-releasing hormone (GnRH) and gonadotrophins.
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An Efficient Method for Extracting Human Fallopian Tube Epithelia for Single-cell Analyses
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Increased Local Testosterone Levels Alter Human Fallopian Tube mRNA Profile and Signaling.

Angela Russo1, Brian P Cain2, Tia Jackson-Bey1

  • 1Department of Pharmaceutical Sciences, University of Illinois Chicago, Chicago, IL 60607, USA.

Cancers
|April 13, 2023
PubMed
Summary
This summary is machine-generated.

Testosterone increases the invasion and migration of fallopian tube epithelial cells (FTECs), potentially contributing to ovarian cancer development. This effect is reversed by androgen receptor antagonists, highlighting a new therapeutic target.

Keywords:
WNT4fallopian tubemicrofluidicsovarian cancertestosterone

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Area of Science:

  • Reproductive biology
  • Gynecologic oncology
  • Endocrinology

Background:

  • Fallopian tube epithelium (FTE) is crucial for reproduction and a potential origin site for High Grade Serous Ovarian Carcinoma (HGSOC).
  • Testosterone, an androgen, promotes oviductal cell proliferation and is implicated in the ovary-FTSEC signaling axis.
  • Protective measures against ovarian cancer, like salpingectomy, reduce androgen levels, suggesting a role for androgens in HGSOC development.

Purpose of the Study:

  • To investigate the impact of increased testosterone on human fallopian tube epithelium (FTE) and its potential role in HGSOC.
  • To explore the molecular mechanisms by which testosterone influences FTE cell behavior, including migration and invasion.
  • To evaluate novel microfluidic systems for studying FTE responses to hormonal stimuli and cancer progression.

Main Methods:

  • Utilized immortalized human fallopian tube cells (FTSEC) and primary human fallopian tube tissues.
  • Employed RNA sequencing on a SOLO microfluidic platform (MFP) to analyze gene expression changes.
  • Used the PREDICT-Multi Organ System (PREDICT-MOS) microfluidic platform to assess cell migration and invasion through Matrigel, with and without androgen receptor (AR) antagonist bicalutamide.

Main Results:

  • Testosterone upregulated wingless-type MMTV integration family, member 4 (WNT4) and induced migration and invasion in immortalized FTSEC.
  • Testosterone downregulated p53 and its target genes (PAX2, CDK1A/p21, CD82/KAI1) in primary human fallopian tissues.
  • Testosterone enhanced FTE migration and invasion in the PREDICT-MOS system, an effect reversed by bicalutamide; it also increased FTSEC adhesion to ovarian stroma.

Conclusions:

  • Primary human fallopian tube tissues and FTSEC respond to testosterone by altering gene expression related to invasion.
  • Testosterone promotes FTE migration and invasion, suggesting a role in HGSOC pathogenesis.
  • Microfluidic platforms offer a dynamic and effective strategy for studying FTE behavior and hormonal influences in a reproductive cancer context.