Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi
Aim: Acquired docetaxel (DOC) resistance of prostate cancer (PCa) is still a clinical problem. In addition to failure in chemotherapy treatment, it causes tumor recurrence. Therefore, novel and more effective compounds are needed in DOC-resistant PCa treatment. This study aimed to investigate the po...
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| Format: | Article |
| Language: | English |
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Duzce University
2021-08-01
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| Series: | Düzce Tıp Fakültesi Dergisi |
| Subjects: | |
| Online Access: | https://dergipark.org.tr/tr/download/article-file/1725636 |
| _version_ | 1797425142887874560 |
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| author | Süleyman İlhan Ferdi Oguz |
| author_facet | Süleyman İlhan Ferdi Oguz |
| author_sort | Süleyman İlhan |
| collection | DOAJ |
| description | Aim: Acquired docetaxel (DOC) resistance of prostate cancer (PCa) is still a clinical problem. In addition to failure in chemotherapy treatment, it causes tumor recurrence. Therefore, novel and more effective compounds are needed in DOC-resistant PCa treatment. This study aimed to investigate the possible cytotoxic and cell death-inducing activities of thymoquinone (TQ), one of the main active components of Nigella sativa L., on DOC-resistant prostate cancer cells.
Material and Methods: DOC-resistant PC3 cells (DOC-R/PC3) were developed by the continuous culture with increment concentrations of DOC (1-10 nM) until they improved their growth and division abilities. The cell viability was determined by MTT assay. The MuseTM Annexin V & Dead Cell kit was performed to detect apoptotic cell death. Autophagic vacuoles were observed by staining autophagic vacuoles. The levels of LC3I, LC3II and Beclin-1 proteins were investigated via western blot analysis.
Results: TQ inhibited the viability of DOC-R/PC3 cells in a dose- and time-dependent manner (p=0.014). The IC50 value of TQ for DOC-R/PC3 cells was calculated as 60 µM at 72 h. Treatment of TQ did not induce apoptotic cell death in DOC-resistant prostate cancer cells but induced the formation of autophagic vacuoles. Moreover, Beclin-1 and LC3-II protein levels were increased in TQ-treated DOC-R/PC3 cells, however, LC3-I levels were decreased in DOC-R/PC3 cells.
Conclusion: All these results show that TQ may become a new therapeutic target for DOC-resistant prostate cancer in the future. |
| first_indexed | 2024-03-09T08:11:41Z |
| format | Article |
| id | doaj.art-98d8ca00d5b14dec98d8a2244ccb459a |
| institution | Directory Open Access Journal |
| issn | 1307-671X |
| language | English |
| last_indexed | 2024-03-09T08:11:41Z |
| publishDate | 2021-08-01 |
| publisher | Duzce University |
| record_format | Article |
| series | Düzce Tıp Fakültesi Dergisi |
| spelling | doaj.art-98d8ca00d5b14dec98d8a2244ccb459a2023-12-02T23:13:25ZengDuzce UniversityDüzce Tıp Fakültesi Dergisi1307-671X2021-08-0123218719110.18678/dtfd.92523897Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesiSüleyman İlhan0Ferdi Oguz1MANISA CELAL BAYAR UNIVERSITYMANISA CELAL BAYAR UNIVERSITYAim: Acquired docetaxel (DOC) resistance of prostate cancer (PCa) is still a clinical problem. In addition to failure in chemotherapy treatment, it causes tumor recurrence. Therefore, novel and more effective compounds are needed in DOC-resistant PCa treatment. This study aimed to investigate the possible cytotoxic and cell death-inducing activities of thymoquinone (TQ), one of the main active components of Nigella sativa L., on DOC-resistant prostate cancer cells. Material and Methods: DOC-resistant PC3 cells (DOC-R/PC3) were developed by the continuous culture with increment concentrations of DOC (1-10 nM) until they improved their growth and division abilities. The cell viability was determined by MTT assay. The MuseTM Annexin V & Dead Cell kit was performed to detect apoptotic cell death. Autophagic vacuoles were observed by staining autophagic vacuoles. The levels of LC3I, LC3II and Beclin-1 proteins were investigated via western blot analysis. Results: TQ inhibited the viability of DOC-R/PC3 cells in a dose- and time-dependent manner (p=0.014). The IC50 value of TQ for DOC-R/PC3 cells was calculated as 60 µM at 72 h. Treatment of TQ did not induce apoptotic cell death in DOC-resistant prostate cancer cells but induced the formation of autophagic vacuoles. Moreover, Beclin-1 and LC3-II protein levels were increased in TQ-treated DOC-R/PC3 cells, however, LC3-I levels were decreased in DOC-R/PC3 cells. Conclusion: All these results show that TQ may become a new therapeutic target for DOC-resistant prostate cancer in the future.https://dergipark.org.tr/tr/download/article-file/1725636otofajibeclin-1lc3prostat kanseridirençtimokinonautophagybeclin-1lc3prostate cancerresistancethymoquinone |
| spellingShingle | Süleyman İlhan Ferdi Oguz Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi Düzce Tıp Fakültesi Dergisi otofaji beclin-1 lc3 prostat kanseri direnç timokinon autophagy beclin-1 lc3 prostate cancer resistance thymoquinone |
| title | Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi |
| title_full | Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi |
| title_fullStr | Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi |
| title_full_unstemmed | Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi |
| title_short | Dosetaksel Dirençli Prostat Kanseri Hücrelerinde Timokinon Tarafından Otofajik Hücre Ölümünün İndüklenmesi |
| title_sort | dosetaksel direncli prostat kanseri hucrelerinde timokinon tarafindan otofajik hucre olumunun induklenmesi |
| topic | otofaji beclin-1 lc3 prostat kanseri direnç timokinon autophagy beclin-1 lc3 prostate cancer resistance thymoquinone |
| url | https://dergipark.org.tr/tr/download/article-file/1725636 |
| work_keys_str_mv | AT suleymanilhan dosetakseldirencliprostatkanserihucrelerindetimokinontarafındanotofajikhucreolumununinduklenmesi AT ferdioguz dosetakseldirencliprostatkanserihucrelerindetimokinontarafındanotofajikhucreolumununinduklenmesi |