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Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications
Cyclin-dependent kinase 5 (CDK5) is a unique member of the cyclin-dependent kinase family. CDK5 is activated by binding with its regulatory proteins, mainly p35, and its activation is essential in the development of the central nervous system (CNS) and neurodegeneration. Recently, it has been report...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720211/ https://www.ncbi.nlm.nih.gov/pubmed/31395805 http://dx.doi.org/10.3390/ijms20163881 |
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author | Oner, Muhammet Lin, Eugene Chen, Mei-Chih Hsu, Fu-Ning Shazzad Hossain Prince, G M Chiu, Kun-Yuan Teng, Chieh-Lin Jerry Yang, Tsung-Ying Wang, Hsin-Yi Yue, Chia-Herng Yu, Ching-Han Lai, Chih-Ho Hsieh, Jer-Tsong Lin, Ho |
author_facet | Oner, Muhammet Lin, Eugene Chen, Mei-Chih Hsu, Fu-Ning Shazzad Hossain Prince, G M Chiu, Kun-Yuan Teng, Chieh-Lin Jerry Yang, Tsung-Ying Wang, Hsin-Yi Yue, Chia-Herng Yu, Ching-Han Lai, Chih-Ho Hsieh, Jer-Tsong Lin, Ho |
author_sort | Oner, Muhammet |
collection | PubMed |
description | Cyclin-dependent kinase 5 (CDK5) is a unique member of the cyclin-dependent kinase family. CDK5 is activated by binding with its regulatory proteins, mainly p35, and its activation is essential in the development of the central nervous system (CNS) and neurodegeneration. Recently, it has been reported that CDK5 plays important roles in regulating various biological and pathological processes, including cancer progression. Concerning prostate cancer, the androgen receptor (AR) is majorly involved in tumorigenesis, while CDK5 can phosphorylate AR and promotes the proliferation of prostate cancer cells. Clinical evidence has also shown that the level of CDK5 is associated with the progression of prostate cancer. Interestingly, inhibition of CDK5 prevents prostate cancer cell growth, while drug-triggered CDK5 hyperactivation leads to apoptosis. The blocking of CDK5 activity by its small interfering RNAs (siRNA) or Roscovitine, a pan-CDK inhibitor, reduces the cellular AR protein level and triggers the death of prostate cancer cells. Thus, CDK5 plays a crucial role in the growth of prostate cancer cells, and AR regulation is one of the important pathways. In this review paper, we summarize the significant studies on CDK5-mediated regulation of prostate cancer cells. We propose that the CDK5–p35 complex might be an outstanding candidate as a diagnostic marker and potential target for prostate cancer treatment in the near future. |
format | Online Article Text |
id | pubmed-6720211 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-67202112019-10-30 Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications Oner, Muhammet Lin, Eugene Chen, Mei-Chih Hsu, Fu-Ning Shazzad Hossain Prince, G M Chiu, Kun-Yuan Teng, Chieh-Lin Jerry Yang, Tsung-Ying Wang, Hsin-Yi Yue, Chia-Herng Yu, Ching-Han Lai, Chih-Ho Hsieh, Jer-Tsong Lin, Ho Int J Mol Sci Review Cyclin-dependent kinase 5 (CDK5) is a unique member of the cyclin-dependent kinase family. CDK5 is activated by binding with its regulatory proteins, mainly p35, and its activation is essential in the development of the central nervous system (CNS) and neurodegeneration. Recently, it has been reported that CDK5 plays important roles in regulating various biological and pathological processes, including cancer progression. Concerning prostate cancer, the androgen receptor (AR) is majorly involved in tumorigenesis, while CDK5 can phosphorylate AR and promotes the proliferation of prostate cancer cells. Clinical evidence has also shown that the level of CDK5 is associated with the progression of prostate cancer. Interestingly, inhibition of CDK5 prevents prostate cancer cell growth, while drug-triggered CDK5 hyperactivation leads to apoptosis. The blocking of CDK5 activity by its small interfering RNAs (siRNA) or Roscovitine, a pan-CDK inhibitor, reduces the cellular AR protein level and triggers the death of prostate cancer cells. Thus, CDK5 plays a crucial role in the growth of prostate cancer cells, and AR regulation is one of the important pathways. In this review paper, we summarize the significant studies on CDK5-mediated regulation of prostate cancer cells. We propose that the CDK5–p35 complex might be an outstanding candidate as a diagnostic marker and potential target for prostate cancer treatment in the near future. MDPI 2019-08-09 /pmc/articles/PMC6720211/ /pubmed/31395805 http://dx.doi.org/10.3390/ijms20163881 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Oner, Muhammet Lin, Eugene Chen, Mei-Chih Hsu, Fu-Ning Shazzad Hossain Prince, G M Chiu, Kun-Yuan Teng, Chieh-Lin Jerry Yang, Tsung-Ying Wang, Hsin-Yi Yue, Chia-Herng Yu, Ching-Han Lai, Chih-Ho Hsieh, Jer-Tsong Lin, Ho Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title | Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title_full | Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title_fullStr | Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title_full_unstemmed | Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title_short | Future Aspects of CDK5 in Prostate Cancer: From Pathogenesis to Therapeutic Implications |
title_sort | future aspects of cdk5 in prostate cancer: from pathogenesis to therapeutic implications |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6720211/ https://www.ncbi.nlm.nih.gov/pubmed/31395805 http://dx.doi.org/10.3390/ijms20163881 |
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