scholarly journals Cytotoxic Effects of Functional Foods Momordica charantia L. and Lycium barbarum L. Extracts on Prostate Cancer Cells

Proceedings ◽  
2017 ◽  
Vol 1 (10) ◽  
pp. 1044 ◽  
Author(s):  
Guzide Satir Basaran ◽  
Hatice Bekci ◽  
Ayse Baldemir ◽  
Selen İlgün ◽  
Ahmet Cumaoğlu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Functional Foods ◽  
Momordica Charantia ◽  
Prostate Cancer Cells ◽  
Lycium Barbarum ◽  
Cytotoxic Effects

Excelsanone, a new isoflavonoid from Erythrina excelsa (Fabaceae), with in vitro antioxidant and in vitro cytotoxic effects on prostate cancer cells lines

2018 ◽  
Vol 34 (5) ◽  
pp. 659-667 ◽  
Author(s):  
Abel Joël Yaya Gbaweng ◽  
Hadidjatou Daïrou ◽  
Stephane Zingué ◽  
Talla Emmanuel ◽  
Alembert Tiabou Tchinda ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Cytotoxic Effects

scholarly journals Melatonin Analogue Antiproliferative and Cytotoxic Effects on Human Prostate Cancer Cells

2018 ◽  
Vol 19 (5) ◽  
pp. 1505 ◽  
Author(s):  
Angela Calastretti ◽  
Giuliana Gatti ◽  
Valeria Lucini ◽  
Silvana Dugnani ◽  
Gianfranco Canti ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cytotoxic Effects

Antiproliferative, antiandrogenic and cytotoxic effects of novel caffeic acid derivatives in LNCaP human androgen-dependent prostate cancer cells

2013 ◽  
Vol 21 (22) ◽  
pp. 7182-7193 ◽  
Author(s):  
J. Thomas Sanderson ◽  
Hélène Clabault ◽  
Cody Patton ◽  
Grégoire Lassalle-Claux ◽  
Jacques Jean-François ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Prostate Cancer Cells ◽  
Cytotoxic Effects ◽  
Caffeic Acid Derivatives

scholarly journals Upregulation of pERK and c-JUN by γ-tocotrienol and not α-tocopherol are essential to the differential effect on apoptosis in prostate cancer cells.

2020 ◽  
Author(s):  
Christine Moore ◽  
Victoria Palau ◽  
Rashid Mahboob ◽  
Janet Lightner ◽  
William Stone ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Cytotoxic Effects ◽  
Jnk Pathway ◽  
Androgen Sensitivity ◽  
Apoptotic Effect ◽  
Select Trial

Abstract Background: α-tocopherol (AT) and γ-tocotrienol (GT3) are vitamin E isoforms considered to have potential chemopreventive properties. AT has been widely studied in vitro and in clinical trials with mixed results. The latest clinical study (SELECT trial) tested AT in prostate cancer patients, determined that AT provided no benefit, and could promote cancer. Conversely, GT3 has shown antineoplastic properties in several in vitro studies, with no clinical studies published to date. GT3 causes apoptosis via upregulation of the JNK pathway; however, inhibition results in a partial block of cell death. We compared side by side the mechanistic differences in these cells in response to AT and GT3.Methods: The effects of GT3 and AT were studied on androgen sensitive LNCaP and androgen independent PC-3 prostate cancer cells. Their cytotoxic effects were analyzed via MTT and confirmed by metabolic assays measuring ATP. Cellular pathways were studied by immunoblot. Quantitative analysis and the determination of relationships between cell signaling events were analyzed for both agents tested. Non-cancerous prostate RWPE-1 cells were also included as a control. Results: The RAF/RAS/ERK pathway was significantly activated by GT3 in LNCaP and PC-3 cells but not by AT. This activation is essential for the apoptotic affect by GT3 as demonstrated the complete inhibition of apoptosis by MEK1 inhibitor U0126. Phospho-c-JUN was upregulated by GT3 but not AT. No changes were observed on AKT for either agent, and no release of cytochrome c into the cytoplasm was detected. Caspases 9 and 3 were efficiently activated by GT3 on both cell lines irrespective of androgen sensitivity, but not in cells dosed with AT. Cell viability of non-cancerous RWPE-1 cells was affected neither by GT3 nor AT. Conclusions: c-JUN is a recognized master regulator of apoptosis as shown previously in prostate cancer. However, the mechanism of action of GT3 in these cells also include a significant activation of ERK which is essential for the apoptotic effect of GT3. The activation of both, ERK and c-JUN, is required for apoptosis and may suggest a relevant step in ensuring circumvention of mechanisms of resistance related to the constitutive activation of MEK1.

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