A facile composite nanoparticle promoted by photoelectron transfer and consumption for tumor combination therapy

2020 ◽  
Vol 4 (10) ◽  
pp. 3047-3056
Author(s):  
Yahui Zhang ◽  
Weizhou Sha ◽  
Yang Liu ◽  
Wei Wang ◽  
Zhi Yuan
Keyword(s):  
Membrane Potential ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Membrane Permeabilization ◽  
Lysosomal Membrane ◽  
Lysosomal Membrane Permeabilization ◽  
Composite Nanoparticle ◽  
Mitochondrial Death Pathway

BTCu NPs can cause significant lysosomal membrane permeabilization (LMP) and mitochondrial membrane potential depolarization, thus indicating a lysosomal–mitochondrial death pathway in cancer cells.

Lysosome Inhibitors Enhance the Chemotherapeutic Activity of Doxorubicin in HepG2 Cells

Chemotherapy ◽  
2016 ◽  
Vol 62 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Yuyin Li ◽  
Yuejun Sun ◽  
Lifang Jing ◽  
Jianjun Wang ◽  
Yali Yan ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Hepg2 Cells ◽  
Mitochondrial Membrane ◽  
Inhibitory Effect ◽  
Membrane Permeabilization ◽  
Lysosomal Membrane ◽  
Bafilomycin A1 ◽  
Lysosomal Membrane Permeabilization ◽  
Proliferative Ability

The lysosome inhibitors bafilomycin A1 and chloroquine have both lysosomotropic properties and autophagy inhibition ability, and are promising clinical agents to be used in combination with anticancer drugs. In order to investigate this combination effect, HepG2 cells were treated with bafilomycin A1, chloroquine, or/and doxorubicin, and their proliferative ability, induction of apoptosis, and the changes of lysosomal membrane permeabilization and mitochondrial membrane potential were studied. The results demonstrate that treatment with bafilomycin A1 or chloroquine alone at a relatively low concentration promotes the inhibitory effect of doxorubicin on cell growth and apoptosis. Further studies reveal that bafilomycin A1 and chloroquine promote lysosomal membrane permeabilization and the reduction of mitochondrial membrane potential induced by doxorubicin. Our findings suggest that bafilomycin A1 and chloroquine potentiate the anticancer effect of doxorubicin in hepatic cancer cells and that supplementation of conventional chemotherapy with lysosome inhibitors may provide a more efficient anticancer therapy.

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.

The repopulating cancer cells in melanoma are characterized by increased mitochondrial membrane potential

2016 ◽  
Vol 382 (2) ◽  
pp. 186-194 ◽  
Author(s):  
Don G. Lee ◽  
Beom K. Choi ◽  
Young H. Kim ◽  
Ho S. Oh ◽  
Sang H. Park ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane

scholarly journals Quantitative analysis of mitochondrial membrane potential heterogeneity in unsynchronized and synchronized cancer cells

2020 ◽  
Vol 35 (1) ◽  
Author(s):  
Amandine Rovini ◽  
Kareem Heslop ◽  
Elizabeth G. Hunt ◽  
Morgan E. Morris ◽  
Diana Fang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Quantitative Analysis ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane

Sojucktang induces apoptosis via loss of mitochondrial membrane potential and caspase-3 activation in KLE human endometrial cancer cells

2009 ◽  
Vol 54 (23) ◽  
pp. 4387-4392 ◽  
Author(s):  
Yeon-Suk Oh ◽  
Hee-Young Kwon ◽  
Soo-Jin Jeong ◽  
Ki-Young Park ◽  
Sun-Young Kim ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3

scholarly journals Emodin, isolated and characterized from an endophytic fungus Polyporales sp., induces apoptotic cell death in human lung cancer cells through the loss of mitochondrial membrane potential

2017 ◽  
Vol 6 (5) ◽  
pp. 288-292
Author(s):  
Refaz Ahmad Dar ◽  
◽  
Rabiya Majeed ◽  
Abid Ali sheikh ◽  
Shakeel-u Rehman ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Endophytic Fungus ◽  
Mitochondrial Membrane ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Close Relative ◽  
Dependent Manner

Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a Chinese herbal anthraquinone that exhibits numerous biological activities, such as antitumor, antibacterial, antiinflammatory, and immunosuppressive. From an endophytic fungus, a close relative of Polyporales sp., found in association with Rheum emodi, Wall. ex Meissn a compound (Rz) was isolated and characterizedby different spectroscopic techniques (1H-NMR, 13CNMR, 2D-NMR, and HRMS). The compound (Rz) displayed a range of cytotoxicities against different human cancer cell lines like THP-1(Leukemia), A549 (Lung), NCI-H322 (lung) and Colo-205(colon) at a concentration of 70 and 100 µM. The compound had strong anticancer activity by arresting the cell cycle at G1 and G2/M phase and loss of mitochondrial membrane potential in A-549 lung cancer cells in concentration dependent manner. The study suggests that emodin induced anticancer effects may have novel therapeutic applications for the treatment of lung cancer.

scholarly journals The Novel Curcumin Derivative 1g Induces Mitochondrial and ER-Stress-Dependent Apoptosis in Colon Cancer Cells by Induction of ROS Production

2020 ◽  
Author(s):  
Hao Wang ◽  
Jia-Lin Sun ◽  
Ying-Xing Xu ◽  
Zhong-Guo Sui
Keyword(s):  
Colon Cancer ◽  
Membrane Potential ◽  
Er Stress ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Colon Cancer Cells ◽  
Ros Scavenging ◽  
Stress Dependent

Abstract Background: A novel curcumin (Cur) derivative 1g can inhibit the proliferation of colon cancer in vitro and in vivo. The purpose of this study was to explore the role of 1g in inducing apoptosis of colon cancer cells, especially mitochondrial apoptosis and endoplasmic reticulum (ER)-stress caused by reactive oxygen species (ROS).Methods: Bioinformatics was used to analyze differentially expressed mrnas. Gene expression was measured by using qRT-PCR and protein expression was measured by using western blotting. Cell apoptosis, cycle, mitochondrial membrane potential and ROS were analyzed by flow cytometry. Experiments on transplanted tumors in animals.Results: The mechanism of this effect was a change in mitochondrial membrane potential caused by 1g that increased its pro-apoptotic activity. In addition, 1g produced ROS, induced G1 checkpoint blockade, and enhanced ER-stress in colon cancer cells. On the contrary, pretreatment with the ROS scavenging agent N-acetyl-l-cysteine (NAC) inhibited the mitochondrial dysfunction caused by 1g and reversed ER-stress, cell cycle stagnation, and apoptosis. Additionally, pretreatment with the p-PERK inhibitor GSK2606414 significantly reduced ER-stress and reversed the apoptosis induced by colon cancer cells.Conclusions: This study not only found that 1g inherits the safety of Cur and has a more inhibitory effect on colon cancer cells than Cur, but also revealed that excessive production of ROS is one of the mechanisms of anti-tumor action.

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