Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines
Abstract Background The androgen receptor (AR) has been studied as an approach to cancer therapy. Aims We used human breast cancer‐derived cells with high, low, and very low expression levels of AR, in addition to prostate cancer‐derived LNCaP and DU‐145 cells as a positive and negative controls to...
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Format: | Article |
Language: | English |
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Wiley
2024-01-01
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Series: | Cancer Reports |
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Online Access: | https://doi.org/10.1002/cnr2.1922 |
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author | Mazdak Jamshidi Fatemeh Keshavarzi Sabrieh Amini Ismail Laher Ali Gheysarzadeh Kambiz Davari |
author_facet | Mazdak Jamshidi Fatemeh Keshavarzi Sabrieh Amini Ismail Laher Ali Gheysarzadeh Kambiz Davari |
author_sort | Mazdak Jamshidi |
collection | DOAJ |
description | Abstract Background The androgen receptor (AR) has been studied as an approach to cancer therapy. Aims We used human breast cancer‐derived cells with high, low, and very low expression levels of AR, in addition to prostate cancer‐derived LNCaP and DU‐145 cells as a positive and negative controls to examine apoptosis caused by a synthetic peptide that targets ARs. Methods and Results The peptide was produced to inhibit AR transactivation in breast cancer cell lines. We then measured cell viability, caspase‐3 activity, and the ratio of Bax/Bcl‐2. The findings indicated that the peptide (100–500 nM) in the presence of dihydrotestosterone (DHT) reduced cell growth in cells with high and low expression level of AR (p < .001), but not in cells with very low levels of AR. Treatment with 100–500 nM of peptide activated caspase‐3 and increased the ratio of Bax/Bcl‐2 in cells with high and low expression levels of AR. Also, increasing concentrations of the peptide (100–500 nM) reduced BrdU incorporation in the presence of DHT and promoted apoptosis in cells with high and low expression levels of AR (p < .001). Conclusion The findings indicate the peptide significantly increased apoptosis in cancer cells. |
first_indexed | 2024-03-08T11:08:28Z |
format | Article |
id | doaj.art-6ba2c6a6a1f24911937e8740d966aea3 |
institution | Directory Open Access Journal |
issn | 2573-8348 |
language | English |
last_indexed | 2024-03-08T11:08:28Z |
publishDate | 2024-01-01 |
publisher | Wiley |
record_format | Article |
series | Cancer Reports |
spelling | doaj.art-6ba2c6a6a1f24911937e8740d966aea32024-01-26T14:25:02ZengWileyCancer Reports2573-83482024-01-0171n/an/a10.1002/cnr2.1922Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell linesMazdak Jamshidi0Fatemeh Keshavarzi1Sabrieh Amini2Ismail Laher3Ali Gheysarzadeh4Kambiz Davari5Department of Biology, Sanandaj Branch Islamic Azad University Sanandaj IranDepartment of Biology, Sanandaj Branch Islamic Azad University Sanandaj IranDepartment of Biology, Sanandaj Branch Islamic Azad University Sanandaj IranDepartment of Anesthesiology, Pharmacology and Therapeutics The University of British Columbia Vancouver British Columbia CanadaDepartment of Clinical Biochemistry Ilam University of Medical Sciences Ilam IranDepartment of Biology, Sanandaj Branch Islamic Azad University Sanandaj IranAbstract Background The androgen receptor (AR) has been studied as an approach to cancer therapy. Aims We used human breast cancer‐derived cells with high, low, and very low expression levels of AR, in addition to prostate cancer‐derived LNCaP and DU‐145 cells as a positive and negative controls to examine apoptosis caused by a synthetic peptide that targets ARs. Methods and Results The peptide was produced to inhibit AR transactivation in breast cancer cell lines. We then measured cell viability, caspase‐3 activity, and the ratio of Bax/Bcl‐2. The findings indicated that the peptide (100–500 nM) in the presence of dihydrotestosterone (DHT) reduced cell growth in cells with high and low expression level of AR (p < .001), but not in cells with very low levels of AR. Treatment with 100–500 nM of peptide activated caspase‐3 and increased the ratio of Bax/Bcl‐2 in cells with high and low expression levels of AR. Also, increasing concentrations of the peptide (100–500 nM) reduced BrdU incorporation in the presence of DHT and promoted apoptosis in cells with high and low expression levels of AR (p < .001). Conclusion The findings indicate the peptide significantly increased apoptosis in cancer cells.https://doi.org/10.1002/cnr2.1922androgen receptoranticancer peptideapoptosisbreast cancerdihydrotestosterone (DHT) |
spellingShingle | Mazdak Jamshidi Fatemeh Keshavarzi Sabrieh Amini Ismail Laher Ali Gheysarzadeh Kambiz Davari Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines Cancer Reports androgen receptor anticancer peptide apoptosis breast cancer dihydrotestosterone (DHT) |
title | Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines |
title_full | Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines |
title_fullStr | Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines |
title_full_unstemmed | Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines |
title_short | Targeting androgen receptor (AR) with a synthetic peptide increases apoptosis in triple negative breast cancer and AR‐expressing prostate cancer cell lines |
title_sort | targeting androgen receptor ar with a synthetic peptide increases apoptosis in triple negative breast cancer and ar expressing prostate cancer cell lines |
topic | androgen receptor anticancer peptide apoptosis breast cancer dihydrotestosterone (DHT) |
url | https://doi.org/10.1002/cnr2.1922 |
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