scholarly journals Low-Dose Valproic Acid Enhances Radiosensitivity of Prostate Cancer through Acetylated p53-Dependent Modulation of Mitochondrial Membrane Potential and Apoptosis

2011 ◽  
Vol 9 (4) ◽  
pp. 448-461 ◽  
Author(s):  
Xufeng Chen ◽  
Jeffrey Y.C. Wong ◽  
Patty Wong ◽  
Eric H. Radany
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Low Dose

Reserpine Induces Apoptosis and Cell Cycle Arrest in Hormone Independent Prostate Cancer Cells through Mitochondrial Membrane Potential Failure

2019 ◽  
Vol 18 (9) ◽  
pp. 1313-1322 ◽  
Author(s):  
Manjula Devi Ramamoorthy ◽  
Ashok Kumar ◽  
Mahesh Ayyavu ◽  
Kannan Narayanan Dhiraviam
Keyword(s):  
Prostate Cancer ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Prostate Cancer Cells

Background: Reserpine, an indole alkaloid commonly used for hypertension, is found in the roots of Rauwolfia serpentina. Although the root extract has been used for the treatment of cancer, the molecular mechanism of its anti-cancer activity on hormonal independent prostate cancer remains elusive. Methods: we evaluated the cytotoxicity of reserpine and other indole alkaloids, yohimbine and ajmaline on Prostate Cancer cells (PC3) using MTT assay. We investigated the mechanism of apoptosis using a combination of techniques including acridine orange/ethidium bromide staining, high content imaging of Annexin V-FITC staining, flow cytometric quantification of the mitochondrial membrane potential and Reactive Oxygen Species (ROS) and cell cycle analysis. Results: Our results indicate that reserpine inhibits DNA synthesis by arresting the cells at the G2 phase and showed all standard sequential features of apoptosis including, destabilization of mitochondrial membrane potential, reduced production of reactive oxygen species and DNA ladder formation. Our in silico analysis further confirmed that indeed reserpine docks to the catalytic cleft of anti-apoptotic proteins substantiating our results. Conclusion: Collectively, our findings suggest that reserpine can be a novel therapeutic agent for the treatment of androgen-independent prostate cancer.

scholarly journals Eya2 Is Overexpressed in Human Prostate Cancer and Regulates Docetaxel Sensitivity and Mitochondrial Membrane Potential through AKT/Bcl-2 Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Zhongyuan Liu ◽  
Long Zhao ◽  
Yongsheng Song
Keyword(s):  
Prostate Cancer ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Cell Lines ◽  
Gleason Score ◽  
Colony Formation ◽  
Mitochondrial Membrane ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Docetaxel Sensitivity

The aberrant expression of Eya2 has been observed in a wide range of cancer types. However, the clinical significance and biological effects of EYA2 in human prostate cancer remain unknown. In this study, we showed that increased levels of Eya2 protein correlated with advanced TNM stage, T stage, and a higher Gleason score. Data from the Cancer Genome Atlas (TCGA) prostate cohort consistently revealed that Eya2 mRNA was positively correlated with a higher Gleason score, higher T stage, and positive nodal metastasis in prostate cancer. Furthermore, data from the Oncomine database showed increased levels of EYA2 mRNA expression in prostate cancer tissues compared with normal tissues. Eya2 protein expression was also higher in prostate cancer cell lines compared with a normal RWPE-1 cell line. We selected LNCaP and PC-3 cell lines for plasmid overexpression and shRNA knockdown. CCK-8, colony formation, and Matrigel invasion assays demonstrated that the overexpression of Eya2 promoted proliferation, colony number, and invasion while Eya2 shRNA inhibited proliferation rate, colony formation, and invasion ability. CCK-8 and Annexin V assays showed that Eya2 reduced sensitivity to docetaxel and docetaxel-induced apoptosis while Eya2 shRNA showed the opposite effects. The overexpression of Eya2 also downregulated the cleavage of caspase3 and PARP while Eya2 depletion upregulated caspase3 and PARP cleavage. Notably, JC-1 staining demonstrated that Eya2 upregulated mitochondrial membrane potential. We further revealed that the overexpression of Eya2 upregulated Bcl-2, matrix metalloproteinase 7 (MMP7), and AKT phosphorylation. Accordingly, data from the TCGA prostate cohort indicated that EYA2 mRNA was positively correlated with the expression of Bcl-2 and MMP7. The inhibition of AKT attenuated EYA2-induced Bcl-2 upregulation. In conclusion, our data demonstrated that Eya2 was upregulated in prostate cancers. EYA2 promotes cell proliferation and invasion as well as cancer progression by regulating docetaxel sensitivity and mitochondrial membrane potential, possibly via the AKT/Bcl-2 axis.

scholarly journals Effects of Medical Diagnostic X-rays Delivered at 0.01 or 0.05 mGy on Human Blood Cells

2021 ◽  
Vol 20 (1) ◽  
pp. 136-144
Author(s):  
Benjamaporn Supawat ◽  
Jongchai Tinlapat ◽  
Rusleena Wongmahamad ◽  
Chuleekorn Silpmuang ◽  
Suchart Kothan ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Blood Cells ◽  
Mitochondrial Membrane ◽  
Low Dose ◽  
Medical Science ◽  
Control Group ◽  
X Rays ◽  
Medical Diagnostic

Background: Low-dose X-rays are commonly used in medical imaging to help in the diagnosis ofdiseases. However, the deleterious effects of exposure to medical diagnostic low-dose X-rays remaina highly debated topic. The objective was to study the effects of medical diagnostic X-rays on humanblood cells. Materials and Methods: We studied the effects of medical diagnostic low-dose X-rays (80kVp), i.e.,0.01 or 0.05 mGy, after the in vitro exposure of human red blood cells (RBCs) and peripheralblood mononucleated cells (PBMCs).Cells with no irradiation served as the control group. The biologicalendpoints that were used to determine the effects of medical diagnostic low-dose X-rays were hemolysisfor RBCs and mitochondrial membrane potential, lysosomes, and the cell cycle for PBMCs. Results: Ourresults showed no changes in the hemolysis of RBCs and mitochondrial membrane potential, lysosome, orcell cycle in cells exposed to these low doses of X-rays when compared to the corresponding nonirradiatedcells at all harvest timepoints. Conclusion: These results suggested that there were no deleterious effectsof diagnostic low-dose X-rays when human RBCs and PBMCs were exposed in vitro. Bangladesh Journal of Medical Science Vol.20(1) 2021 p.136-144

Low dose (−)deprenyl is cytoprotective: It maintains mitochondrial membrane potential and eliminates oxygen radicals

Life Sciences ◽  
2005 ◽  
Vol 78 (3) ◽  
pp. 225-231 ◽  
Author(s):  
L. Simon ◽  
G. Szilágyi ◽  
Z. Bori ◽  
G. Telek ◽  
K. Magyar ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Oxygen Radicals ◽  
Low Dose

scholarly journals Xiaoyaosan Decoction, a Traditional Chinese Medicine, Inhibits Oxidative-Stress-Induced Hippocampus Neuron Apoptosis In Vitro

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Zhen-zhi Meng ◽  
Jing-hong Hu ◽  
Jia-xu Chen ◽  
Guang-xin Yue
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Low Dose ◽  
Free Calcium ◽  
High Dose ◽  
Hippocampus Neuron ◽  
Neuron Apoptosis

Xiaoyaosan (XYS) decoction is a famous prescription for the treatment of mental disorders in China. In this experiment, we explored the way in which XYS decoction-reverse hippocampus neuron apoptosis in vitro. We used XYS decoction-containing serum to treat oxidative-stress-induced hippocampus neuron apoptosis and used immunofluorescence to determine the concentration of free calcium, mitochondrial membrane potential, and apoptotic rate of neuron. Results showed that 3-hour oxidative stress decrease mitochondrial membrane potential, increase the concentration of free calcium and apoptotic rate of neuron via triggering pathological changes of nucleus such as karyorrhexis, karyopyknosis. Low, medium, high dose of XYS-decoction-containing serum could reverse these phenomenon, and the effect of low-dose XYS-decoction-containing serum was significant in improving mitochondrial membrane potential and apoptotic rate of neuron. These findings suggest that XYS decoction may be helpful in reducing oxidative-stress-induced hippocampus neuron apoptosis.

scholarly journals Shikonin Enhances the Antitumor Effect of Cabazitaxel in Prostate Cancer Stem Cells and Reverses Cabazitaxel Resistance by Inhibiting the Expression of ABCG2 and ALDH3A1

2020 ◽  
Author(s):  
Lili Wang ◽  
Birgit Stadlbauer ◽  
Chen Lyu ◽  
Alexander Buchner ◽  
Heike Pohla
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Membrane Potential ◽  
Cancer Stem Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Antitumor Effect ◽  
Migration And Invasion ◽  
Drug Resistant ◽  
Resistant Cells

Abstract Background: Cancer stem cells (CSCs) are a small population among cancer cells, defined as capable of self-renewal, and driving tumor growth, metastasis, and therapeutic relapse. The development of therapeutic strategies to target CSCs is of great importance to prevent tumor metastasis and relapse. Increasing evidence shows that shikonin has inhibiting effects on CSCs. This study was to determine the effect of shikonin on prostate CSCs, and on drug resistant cells.Methods: Sphere formation assay was used to enrich prostate CSCs. The effect of shikonin on viability, proliferation, migration, and invasion was studied. Typical CSCs markers were analyzed by flow cytometry and RT-qPCR. The cytotoxic mechanism of shikonin was analyzed by staining for annexin V, reactive oxygen species (ROS) and mitochondrial membrane potential. To study the effect of shikonin on drug resistant cells a cabazitaxel resistant cell line was established.Results: Shikonin inhibited the viability, proliferation, migration, and invasion of prostate CSCs. Shikonin enhanced the antitumor effect of cabazitaxel, which is a second-line chemotherapeutic drug in advanced prostate cancer. Shikonin induced apoptosis through generating ROS and disrupting the mitochondrial membrane potential. Furthermore, shikonin suppressed the expression of ALDH3A1 and ABCG2 in prostate CSCs, which are two markers related to drug-resistance. When inhibiting the expression of ABCG2 and ALDH3A1, the cabazitaxel resistant cells acquired more sensibility to cabazitaxel. Conclusions: Shikonin enhances the cytotoxic activity of cabazitaxel in prostate CSCs and reverses the cabazitaxel-resistant state.

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