Prostate Cancer Stem Cells: Biology and Treatment Implications

Stem cells differentiate into mature organ/tissue-specific cells at a steady pace under normal conditions, but their growth can be accelerated during the process of tissue healing or in the context of certain diseases. It is postulated that the proliferation and growth of carcinomas are sustained by...

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Main Authors: Ioannis M. Koukourakis, Kalliopi Platoni, Vassilis Kouloulias, Stella Arelaki, Anna Zygogianni
Format: Article
Language:English
Published: MDPI AG 2023-10-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/19/14890
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author Ioannis M. Koukourakis
Kalliopi Platoni
Vassilis Kouloulias
Stella Arelaki
Anna Zygogianni
author_facet Ioannis M. Koukourakis
Kalliopi Platoni
Vassilis Kouloulias
Stella Arelaki
Anna Zygogianni
author_sort Ioannis M. Koukourakis
collection DOAJ
description Stem cells differentiate into mature organ/tissue-specific cells at a steady pace under normal conditions, but their growth can be accelerated during the process of tissue healing or in the context of certain diseases. It is postulated that the proliferation and growth of carcinomas are sustained by the presence of a vital cellular compartment resembling stem cells residing in normal tissues: ‘stem-like cancer cells’ or cancer stem cells (CSCs). Mutations in prostate stem cells can lead to the formation of prostate cancer. Prostate CSCs (PCSCs) have been identified and partially characterized. These express surface markers include CD44, CD133, integrin α2β1, and pluripotency factors like OCT4, NANOG, and SOX2. Several signaling pathways are also over-activated, including Notch, PTEN/Akt/PI3K, RAS-RAF-MEK-ERK and HH. Moreover, PCSCs appear to induce resistance to radiotherapy and chemotherapy, while their presence has been linked to aggressive cancer behavior and higher relapse rates. The development of treatment policies to target PCSCs in tumors is appealing as radiotherapy and chemotherapy, through cancer cell killing, trigger tumor repopulation via activated stem cells. Thus, blocking this reactive stem cell mobilization may facilitate a positive outcome through cytotoxic treatment.
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spelling doaj.art-760c19a154c640ee8dcb042bd98fca442023-11-19T14:32:07ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-10-0124191489010.3390/ijms241914890Prostate Cancer Stem Cells: Biology and Treatment ImplicationsIoannis M. Koukourakis0Kalliopi Platoni1Vassilis Kouloulias2Stella Arelaki3Anna Zygogianni4Radiation Oncology Unit, 1st Department of Radiology, Aretaieion Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 11528 Athens, GreeceMedical Physics Unit, 2nd Department of Radiology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 12462 Athens, GreeceRadiation Oncology Unit, 2nd Department of Radiology, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 12462 Athens, GreeceTranslational Functional Cancer Genomics, National Center for Tumor Diseases, German Cancer Research Center, 69120 Heidelberg, GermanyRadiation Oncology Unit, 1st Department of Radiology, Aretaieion Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 11528 Athens, GreeceStem cells differentiate into mature organ/tissue-specific cells at a steady pace under normal conditions, but their growth can be accelerated during the process of tissue healing or in the context of certain diseases. It is postulated that the proliferation and growth of carcinomas are sustained by the presence of a vital cellular compartment resembling stem cells residing in normal tissues: ‘stem-like cancer cells’ or cancer stem cells (CSCs). Mutations in prostate stem cells can lead to the formation of prostate cancer. Prostate CSCs (PCSCs) have been identified and partially characterized. These express surface markers include CD44, CD133, integrin α2β1, and pluripotency factors like OCT4, NANOG, and SOX2. Several signaling pathways are also over-activated, including Notch, PTEN/Akt/PI3K, RAS-RAF-MEK-ERK and HH. Moreover, PCSCs appear to induce resistance to radiotherapy and chemotherapy, while their presence has been linked to aggressive cancer behavior and higher relapse rates. The development of treatment policies to target PCSCs in tumors is appealing as radiotherapy and chemotherapy, through cancer cell killing, trigger tumor repopulation via activated stem cells. Thus, blocking this reactive stem cell mobilization may facilitate a positive outcome through cytotoxic treatment.https://www.mdpi.com/1422-0067/24/19/14890prostate cancerstem cellsradiotherapychemotherapy
spellingShingle Ioannis M. Koukourakis
Kalliopi Platoni
Vassilis Kouloulias
Stella Arelaki
Anna Zygogianni
Prostate Cancer Stem Cells: Biology and Treatment Implications
International Journal of Molecular Sciences
prostate cancer
stem cells
radiotherapy
chemotherapy
title Prostate Cancer Stem Cells: Biology and Treatment Implications
title_full Prostate Cancer Stem Cells: Biology and Treatment Implications
title_fullStr Prostate Cancer Stem Cells: Biology and Treatment Implications
title_full_unstemmed Prostate Cancer Stem Cells: Biology and Treatment Implications
title_short Prostate Cancer Stem Cells: Biology and Treatment Implications
title_sort prostate cancer stem cells biology and treatment implications
topic prostate cancer
stem cells
radiotherapy
chemotherapy
url https://www.mdpi.com/1422-0067/24/19/14890
work_keys_str_mv AT ioannismkoukourakis prostatecancerstemcellsbiologyandtreatmentimplications
AT kalliopiplatoni prostatecancerstemcellsbiologyandtreatmentimplications
AT vassiliskouloulias prostatecancerstemcellsbiologyandtreatmentimplications
AT stellaarelaki prostatecancerstemcellsbiologyandtreatmentimplications
AT annazygogianni prostatecancerstemcellsbiologyandtreatmentimplications