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Study · In vitro (cells) · 2000

6 results

Luteinizing hormone-releasing hormone induces nuclear factor kappaB-activation and inhibits apoptosis in ovarian cancer cells.

Gründker C, Schulz K, Günthert AR, Emons G

The Journal of clinical endocrinology and metabolism1 Oct 2000Cited by 47 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In ovarian cancer cells, triptorelin did not induce apoptosis.

    In plain wordsIn cells, triptorelin did not induce programmed cell death.

    Outcome
    No significant changeApoptosis induction
    Study

    humann: not reported in source

    EFO-21 and EFO-27 ovarian cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Apoptosis induction by Triptorelin was never observed.
    1 context sentence
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.
  2. 02LabIn vitro (cells)Mechanism

    In EFO-21 ovarian cancer cells, triptorelin reduced doxorubicin-induced apoptosis to 17% compared with 31% with doxorubicin alone.

    In plain wordsIn cells, triptorelin reduced doxorubicin-induced cell death to 17%, compared with 31% with doxorubicin alone.

    Outcome
    DecreaseDoxorubicin-induced apoptosis in EFO-21
    Study

    humann: not reported in source

    EFO-21 ovarian cancer cells
    Comparator
    Doxorubicin alone
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    100 nmol/LAs given in this study (human).

    Measurements

    Apoptotic cells
    17%
    EFO-21 with triptorelin and doxorubicin
    Apoptotic cells
    31%
    EFO-21 with doxorubicin alone

    Source sentences

    Summary
    In cultures treated simultaneously with Triptorelin (100 nmol/L), the percentage of apoptotic cells was reduced significantly, to 17% or 18%, respectively (P < 0.001).
    2 context sentences
    Summary · context
    Treatment with Doxorubicin (1 nmol/L) for 72 h increased the percentage of apoptotic cells in EFO-21 and EFO-27 ovarian cancer cell lines to 31% or 34%, respectively.
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.
  3. 03LabIn vitro (cells)Mechanism

    In EFO-27 ovarian cancer cells, triptorelin reduced doxorubicin-induced apoptosis to 18% compared with 34% with doxorubicin alone.

    In plain wordsIn cells, triptorelin reduced doxorubicin-induced cell death to 18%, compared with 34% with doxorubicin alone.

    Outcome
    DecreaseDoxorubicin-induced apoptosis in EFO-27
    Study

    humann: not reported in source

    EFO-27 ovarian cancer cells
    Comparator
    Doxorubicin alone
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    100 nmol/LAs given in this study (human).

    Measurements

    Apoptotic cells
    18%
    EFO-27 with triptorelin and doxorubicin
    Apoptotic cells
    34%
    EFO-27 with doxorubicin alone

    Source sentences

    Summary
    In cultures treated simultaneously with Triptorelin (100 nmol/L), the percentage of apoptotic cells was reduced significantly, to 17% or 18%, respectively (P < 0.001).
    2 context sentences
    Summary · context
    Treatment with Doxorubicin (1 nmol/L) for 72 h increased the percentage of apoptotic cells in EFO-21 and EFO-27 ovarian cancer cell lines to 31% or 34%, respectively.
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.
  4. 04LabIn vitro (cells)Mechanism

    In reporter-transfected EFO-21 ovarian cancer cells, triptorelin increased NFkappaB-induced SEAP expression 5.3-fold.

    In plain wordsIn cells, triptorelin increased NFkappaB reporter activity 5.3-fold compared with no triptorelin.

    Outcome
    IncreaseNFkappaB reporter activation in EFO-21
    Study

    humann: not reported in source

    Reporter-transfected EFO-21 ovarian cancer cells
    Comparator
    Without Triptorelin
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    100 nmol/L · 96 hAs given in this study (human).

    Measurements

    NFkappaB-induced SEAP expression
    5.3 fold
    EFO-21

    Source sentences

    Summary
    When EFO-21 or EFO-27 cells were transfected with pNFkappaB-SEAP and subsequently treated with Triptorelin (100 nmol/L), NFkappaB-induced SEAP expression increased 5.3-fold or 4.7-fold, respectively (P < 0.001).
    2 context sentences
    Summary · context
    For determination of Triptorelin-induced NFkappaB activation, cells were transfected with a NFkappaB-secreted alkaline phosphatase reporter gene plasmid (pNFkappaB-SEAP) and cultured for 96 h with or without Triptorelin.
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.
  5. 05LabIn vitro (cells)Mechanism

    In reporter-transfected EFO-27 ovarian cancer cells, triptorelin increased NFkappaB-induced SEAP expression 4.7-fold.

    In plain wordsIn cells, triptorelin increased NFkappaB reporter activity 4.7-fold compared with no triptorelin.

    Outcome
    IncreaseNFkappaB reporter activation in EFO-27
    Study

    humann: not reported in source

    Reporter-transfected EFO-27 ovarian cancer cells
    Comparator
    Without Triptorelin
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    100 nmol/L · 96 hAs given in this study (human).

    Measurements

    NFkappaB-induced SEAP expression
    4.7 fold
    EFO-27

    Source sentences

    Summary
    When EFO-21 or EFO-27 cells were transfected with pNFkappaB-SEAP and subsequently treated with Triptorelin (100 nmol/L), NFkappaB-induced SEAP expression increased 5.3-fold or 4.7-fold, respectively (P < 0.001).
    2 context sentences
    Summary · context
    For determination of Triptorelin-induced NFkappaB activation, cells were transfected with a NFkappaB-secreted alkaline phosphatase reporter gene plasmid (pNFkappaB-SEAP) and cultured for 96 h with or without Triptorelin.
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.

Studies that did not test the peptide alone1

In this study, Triptorelin (Trelstar, Decapeptyl) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Triptorelin (Trelstar, Decapeptyl).

  1. 06LabNot a test of Triptorelin (Trelstar, Decapeptyl) aloneIn vitro (cells)Mechanism

    In ovarian cancer cells, SN50 blocked triptorelin's reduction of doxorubicin-induced apoptosis by inhibiting NFkappaB nuclear translocation.

    In plain wordsIn cells, SN50 blocked triptorelin's protection against doxorubicin-induced cell death compared with triptorelin without SN50.

    Outcome
    DecreaseSN50 blockade of antiapoptotic effect
    Study

    humann: not reported in source

    EFO-21 and EFO-27 ovarian cancer cells
    Comparator
    Triptorelin without SN50
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Triptorelin-induced reduction of Doxorubicin-induced apoptosis was blocked by SN50-mediated inhibition of NFkappaB translocation into the nucleus.
    1 context sentence
    Summary · context
    EFO-21 and EFO-27 ovarian cancer cells were treated with LHRH agonist Triptorelin or with cytotoxic agent Doxorubicin in the absence or presence of Triptorelin.

    In this study, Triptorelin (Trelstar, Decapeptyl) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Triptorelin (Trelstar, Decapeptyl).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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