The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line

Objective: Senescence may act as an antitumor mechanism by preventing the proliferation of cancer cells. Here we investigated the hypothesis that PC3 prostate cancer cells resistant to bortezomib respond differently to proteasomal inhibition with respect to induction of the senescence program as com...

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Main Authors: Ertan Kanbur, Semih Şeker, Ferah Budak, Azmi Yerlikaya
Format: Article
Language:English
Published: Istanbul University Press 2023-06-01
Series:European Journal of Biology
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Online Access:https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/B218A92BA9454949935DB450BDB7C8DC
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author Ertan Kanbur
Semih Şeker
Ferah Budak
Azmi Yerlikaya
author_facet Ertan Kanbur
Semih Şeker
Ferah Budak
Azmi Yerlikaya
author_sort Ertan Kanbur
collection DOAJ
description Objective: Senescence may act as an antitumor mechanism by preventing the proliferation of cancer cells. Here we investigated the hypothesis that PC3 prostate cancer cells resistant to bortezomib respond differently to proteasomal inhibition with respect to induction of the senescence program as compared to the parental cells. Materials and Methods: The degree of senescence was measured by 𝛽-galactosidase activity and the level of senescenceassociated p16 INK4a by Western blotting after treatment of cells with varying concentrations of bortezomib. In addition, the senescence-associated secretory phenotype was analyzed by Human Cytokine Antibody Array. Results: It is reported that the basal level of senescence was lower in resistant cells compared to non-resistant cells. It was found that the basal level of the senescence marker p16 INK4a was lower in bortezomib-resistant cells than in parent non-resistant cells. Moreover, p16 INK4a was significantly reduced in both cells under conditions of 100 nM bortezomib treatment, a finding suggesting that the reduced senescence after proteasomal inhibition was likely due to the reduced levels of p16 INK4a. Finally, it is reported here for the first time that basal levels of the proteins NAP2, FGF-6, MIP-3𝛼, and PARC are significantly increased in the resistant cells compared to the parental cells. Conclusion: Overall, the results suggest that inhibition of senescence may play an important function in the development of resistance to bortezomib.
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issn 2618-6144
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spelling doaj-art-ce48d59a6e514019be26041b3736bfc22025-08-20T03:48:45ZengIstanbul University PressEuropean Journal of Biology2618-61442023-06-01821495810.26650/EurJBiol.2023.11240253123456The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell LineErtan Kanbur0https://orcid.org/0000-0001-8399-8942Semih Şeker1https://orcid.org/0000-0002-8957-2050Ferah Budak2https://orcid.org/0000-0001-7625-9148Azmi Yerlikaya3https://orcid.org/0000-0002-0678-0701Erciyes Üniversitesi, Kayseri, TurkiyeKütahya Sağlık Bilimleri Üniversitesi, Kutahya, TurkiyeBursa Uludağ Üniversitesi, Bursa, TürkiyeKütahya Sağlık Bilimleri Üniversitesi, Kutahya, TurkiyeObjective: Senescence may act as an antitumor mechanism by preventing the proliferation of cancer cells. Here we investigated the hypothesis that PC3 prostate cancer cells resistant to bortezomib respond differently to proteasomal inhibition with respect to induction of the senescence program as compared to the parental cells. Materials and Methods: The degree of senescence was measured by 𝛽-galactosidase activity and the level of senescenceassociated p16 INK4a by Western blotting after treatment of cells with varying concentrations of bortezomib. In addition, the senescence-associated secretory phenotype was analyzed by Human Cytokine Antibody Array. Results: It is reported that the basal level of senescence was lower in resistant cells compared to non-resistant cells. It was found that the basal level of the senescence marker p16 INK4a was lower in bortezomib-resistant cells than in parent non-resistant cells. Moreover, p16 INK4a was significantly reduced in both cells under conditions of 100 nM bortezomib treatment, a finding suggesting that the reduced senescence after proteasomal inhibition was likely due to the reduced levels of p16 INK4a. Finally, it is reported here for the first time that basal levels of the proteins NAP2, FGF-6, MIP-3𝛼, and PARC are significantly increased in the resistant cells compared to the parental cells. Conclusion: Overall, the results suggest that inhibition of senescence may play an important function in the development of resistance to bortezomib.https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/B218A92BA9454949935DB450BDB7C8DCbortezomibcancerprostateproteasomep16 ink4asenescence
spellingShingle Ertan Kanbur
Semih Şeker
Ferah Budak
Azmi Yerlikaya
The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
European Journal of Biology
bortezomib
cancer
prostate
proteasome
p16 ink4a
senescence
title The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
title_full The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
title_fullStr The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
title_full_unstemmed The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
title_short The Senescence Program is Reduced in Proteasome Inhibitor Bortezomib-Resistant PC3 Prostate Cancer Cell Line
title_sort senescence program is reduced in proteasome inhibitor bortezomib resistant pc3 prostate cancer cell line
topic bortezomib
cancer
prostate
proteasome
p16 ink4a
senescence
url https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/B218A92BA9454949935DB450BDB7C8DC
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