Evidence map›Paper›PMID 14534535›Full record

ArticleOncogene2003

Progesterone-induced apoptosis in immortalized normal and malignant human ovarian surface epithelial cells involves enhanced expression of FasL.

Viqar Syed, Shuk-Mei Ho

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Depot-Medroxyprogesterone Acetate Use Is Associated with Decreased Risk of Ovarian Cancer: The Mounting Evidence of a Protective Role of Progestins.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Progesterone action in breast, uterine, and ovarian cancers.Journal of molecular endocrinology · 2015
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Estrous cycle modulates ovarian carcinoma growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Viqar SyedDepartment of Surgery, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Shuk-Mei Ho
University of Massachusetts Chan Medical School · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
CYP1A1, estrogen metabolism and ovarian carcinogenesisR01CA094221 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HO, SHUK-MEI · 2002 to 2004
$935k
Molecular Mechanism of Neoplastic TransformationR03CA091250 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SYED, VIQAR · 2002 to 2003
$159k
NCI NIH HHS CA091250NCI NIH HHS CA94221NIDDK NIH HHS P30 DK32520
6 · The paper itself

Abstract

Progesterone (P4) has been implicated as a protective factor for epithelial ovarian cancers, yet little is known about its mechanism of action. We previously reported that pregnancy-equivalent doses of P4 inhibited the growth of normal and malignant human ovarian surface epithelial (HOSE) cells. Here, we investigated how P4-induced cell death in two immortalized normal (HOSE 642, HOSE 12-12) and two malignant (OVCA 429, OVCA 432) HOSE cell lines. The exposure of HOSE or OVCA cell cultures to 10(-6) M P4 induced time-dependent increases in early and late apoptotic cells and activation of caspase-8 and -3, but not that of caspase-9. A general caspase inhibitor Z-VAD effectively blocked the P4-induced cell death in a dose-dependent manner. Comparable levels of Fas mRNA and protein were expressed in HOSE and OVCA cell lines, and these levels were unaffected by P4. In contrast, levels of FasL mRNA and protein were higher in OVCA cells than in HOSE cells. Interestingly, the hormone enhanced levels of FasL mRNA and protein in HOSE cells, but lowered their levels in OVCA cells. The exposure of HOSE or OVCA cells to an activating anti-Fas antibody induced cell loss, whereas treatment of cells with a blocking anti-FasL antibody reduced the P4-induced cell loss. Cotreatment of cells with the activating anti-Fas antibody and P4 produced additive effects on cell loss. These results reveal for the first time that P4 induces apoptosis in HOSE and OVCA cells via activation of a caspase-8-initiated Fas/FasL signaling pathway. They also demonstrate differential P4-regulation of FasL expression between HOSE and OVCA cells.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAdultAmino Acid Chloromethyl KetonesApoptosisCaspase 8Caspase 9CaspasesCell DivisionDose-Response Relationship, DrugDrug Therapy, CombinationEnzyme ActivationEnzyme InhibitorsEpithelial CellsFas Ligand ProteinFemaleAmino Acid Chloromethyl Ketonesbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCASP8 protein, humanCASP9 protein, humanCaspase 8Caspase 9CaspasesEnzyme InhibitorsFASLG protein, humanFas Ligand ProteinMembrane GlycoproteinsProgesterone

Identifiers

PMID14534535
OpenAlexW2087590552

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.