Cobalt(ii) 8-hydroxyquinoline complexes: structure, cytotoxicity and action mechanism

MedChemComm ◽  
2016 ◽  
Vol 7 (5) ◽  
pp. 806-812 ◽  
Author(s):  
Hai-Rong Zhang ◽  
Ke-Bin Huang ◽  
Zhen-Feng Chen ◽  
Yan-Cheng Liu ◽  
You-Nian Liu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Proliferation Inhibition ◽  
Inhibition Activity ◽  
Action Mechanism ◽  
Cancer Cell Apoptosis

Three cobalt(ii) complexes with 8-hydroxyquinoline derivatives as ligands were synthesized. They exhibited strong proliferation inhibition activity against T-24 cancer cells, which induced cancer cell apoptosis via intrinsic caspase-mitochondria pathways.

scholarly journals Combination of chemotherapy and oxidative stress to enhance cancer cell apoptosis

2020 ◽  
Vol 11 (12) ◽  
pp. 3215-3222
Author(s):  
Xinming Li ◽  
Yanan Hou ◽  
Jintao Zhao ◽  
Jin Li ◽  
Song Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cancer Cell Apoptosis ◽  
And Oxidative Stress

The 1,2-diselenolane unit is a general scaffold to construct glutathione-dependent prodrugs that show increased potency to cancer cells, and work via a combination of chemotherapy and oxidative stress.

scholarly journals Lamprey Immune Protein Mediates Apoptosis of Lung Cancer Cells Via the Endoplasmic Reticulum Stress Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaoping Song ◽  
Xiangting Xu ◽  
Jiali Lu ◽  
Xiaoyuan Chi ◽  
Yue Pang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Lung Cancer Cells ◽  
Stress Signaling ◽  
Lung Cancer Cell ◽  
Cancer Cell Apoptosis ◽  
Stress Signaling Pathway

Lamprey immune protein (LIP), a novel protein derived from the Lampetra japonica, has been shown to exert efficient tumoricidal actions without concomitant damage to healthy cells. Our study aimed to ascertain the mechanisms by which LIP inhibits lung cancer cells, thus delineating potential innovative therapeutic strategies. LIP expression in lung cancer cells was evaluated by western blotting and immunohistochemistry. Functional assays, such as high-content imaging, 3D-structured illumination microscopy (3D-SIM) imaging, flow cytometry, and confocal laser scanning microscopy, were performed to examine the proliferation and lung cancer cell apoptosis. Tumor xenograft assays were performed using an in vivo imaging system. We observed that LIP induces the decomposition of certain lung cancer cell membranes by destroying organelles such as the microtubules, mitochondria, and endoplasmic reticulum (ER), in addition to causing leakage of cytoplasm, making the maintenance of homeostasis difficult. We also demonstrated that LIP activates the ER stress pathway, which mediates lung cancer cell apoptosis by producing reactive oxygen species (ROS). In addition, injection of LIP significantly retarded the tumor growth rate in nude mice. Taken together, these data revealed a role of LIP in the regulation of lung cancer cell apoptosis via control of the ER stress signaling pathway, thus revealing its possible application in lung cancer treatment.

scholarly journals Su1010 – Abnormal Activation of Hnrnpa0 Inhibits Cancer Cell Apoptosis and Promotes Excessive Mitosis in Cancer Cells

2019 ◽  
Vol 156 (6) ◽  
pp. S-484
Author(s):  
Hiroaki Konishi ◽  
Mikihiro Fujiya ◽  
Akemi Kita ◽  
Hiroki Tanaka ◽  
Shin Kashima ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cancer Cell Apoptosis

scholarly journals Effect of drug-loaded microbubbles combined with ultrasound on the apoptosis of cancer cells and the expression of Bax and Bcl-2 in a rabbit VX2 liver tumor model

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Kun Chen ◽  
Liang Zhang
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Condensation Reaction ◽  
Drug Loading ◽  
Mechanical Vibration ◽  
B Cell Lymphoma ◽  
Plga Nanoparticles ◽  
Control Group ◽  
Cancer Cell Apoptosis

Abstract The aim of the present study was to investigate whether the use of drug-loaded microbubbles combined with ultrasound promotes the apoptosis of cancer cells by regulating B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) expression. Adriamycin-loaded PLGA nanoparticles (ADM-NP) were fabricated using a modified emulsification process. Lipid microbubbles (NH2-MB) were prepared by mechanical vibration. The carboxyl groups of ADM-NP and NH2-MB underwent a condensation reaction after 48 h, and adriamycin-loaded PLGA nanoparticles microbubble complexes (ADM-NMC) were obtained. High-performance liquid chromatography demonstrated that the entrapment efficiency and drug loading of ADM-NMC were 85.32 ± 5.41% and 7.91 ± 0.27%, respectively. The VX2 liver cancer model was established in 30 New Zealand rabbits, which were subsequently divided into three groups (n=10): a control group that received 5 ml of saline, an ADM-NP group that received 5 ml of ADM-NP and an ADM-NMC group that received 5 ml of ADM-NMC. Rabbits in the ADM-NP and ADM-NMC groups underwent irradiation 120 s with low frequency ultrasound (1 MHz, 0.5 W/cm2) for 120 s following injection. The echogenicity of tumors markedly increased following ADM-NP and ADM-NMC treatment. Staining with hematoxylin and eosin demonstrated that the tumor shape became more normal in the ADM-NP and ADM-NMC groups compared with the control group. Immunohistochemical staining and Western blotting determined that the expression of Bax increased and the expression of Bcl-2 decreased following treatment with ADM-NP and ADM-NMC. Cancer cell apoptosis was detected by flow cytometry and it was determined that apoptosis significantly increased following treatment with ADM-NP and ADM-NMC (P<0.01). Therefore, the present study demonstrated that the use of drug-loaded microbubbles combined with ultrasound may enhance the efficiency of tumor inhibition. This may be due to the promotion of cancer cell apoptosis via regulation of Bax and Bcl-2 expression.

scholarly journals Encapsulating Anti-Parasite Benzimidazole Drugs into Lipid-Coated Calcium Phosphate Nanoparticles to Efficiently Induce Skin Cancer Cell Apoptosis

2021 ◽  
Vol 3 ◽  
Author(s):  
Fatemeh Movahedi ◽  
Wenyi Gu ◽  
Christiane Pienna Soares ◽  
Zhi Ping Xu
Keyword(s):  
Calcium Phosphate ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Morphological Changes ◽  
Migration Activity ◽  
Primary Tumors ◽  
Cancer Cell Apoptosis ◽  
Tumor Dissemination ◽  
Anti Cancer

Benzimidazole (BMZ) family of anti-worm drugs has been now repurposed as anti-cancer drugs. However, offering a general reformulation method for these drugs is essential due to their hydrophobicity and low aqueous solubility. In this work, we developed a general approach to load typical BMZ drugs as tiny nanocrystals within lipid-coated calcium phosphate (LCP) nanoparticles. BMZ drug-loaded LCP nanoparticles increased their solubility in PBS by 100–200% and significantly enhanced the anti-cancer efficacy in the treatment of B16F0 melanoma cells. These drug-LCP nanoparticles induced much more cancer cell apoptosis, generated much more reactive oxygen species (ROS) and inhibited Bcl-2 expression of cancer cells. Moreover, BMZ drug-loaded LCP nanoparticles caused morphological change and extension disruption of cancer cells, and significantly reduced migration activity, representing high possibility for inhibition of tumor dissemination and metastasis. Very advantageously, BMZ drug-loaded LCP nanoparticles did not show any obvious toxicity, Bcl-2 inhibition and morphological changes in HEK293T healthy cells. In conclusion, BMZ drug-incorporated LCP nanoformulations may be a valuable nanomedicine that is able to inhibit primary tumors and prevent tumor dissemination with minimum side effects on healthy cells and tissues.

scholarly journals 5-Fluorouracil enhances the chemosensitivity of gastric cancer to TRAIL via inhibition of the MAPK pathway

2020 ◽  
Author(s):  
Hui Li ◽  
Jing Lv ◽  
Jing Guo ◽  
Shasha Wang ◽  
Shihai Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Mapk Pathway ◽  
Cell Counting ◽  
Gastric Cancer Cells ◽  
Antitumor Effects ◽  
Cancer Cell Apoptosis

Abstract Background Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has the ability to selectively trigger cancer cell apoptosis and can be used as a target for tumor therapy. However, gastric cancer cells are usually insensitive to TRAIL so reducing this drug resistance may improve the treatment of gastric cancer. Methods In this study, we used Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) experiments to determine the effects of 5-fluorouracil (5-FU) and TRAIL on the proliferation of gastric cancer cells. An Annexin V/propidium iodide (PI) staining experiment was used to detect apoptosis, and Western blotting was used to analyze the expression levels of apoptosis-related proteins and mitogen-activated protein kinase (MAPK) pathway proteins. The antitumor effects of 5-FU and TRAIL were verified in vivo using a nude mouse tumorigenesis experiment, and a TUNEL assay was performed to evaluate apoptosis in tumor tissue from the nude mice. Results The combination of 5-FU and TRAIL had a greater inhibitory effect on the proliferation of gastric cancer cells than 5-FU or TRAIL alone both in vivo and in vitro. 5-FU enhanced TRAIL-induced gastric cancer cell apoptosis by inactivating the MAPK pathway. Conclusion Overall, our analysis provided new insights into the role of 5-FU in increasing sensitivity to TRAIL. 5-FU can be used as a sensitizer for TRAIL, and its administration is a potential strategy for the treatment of gastric cancer.

Caging of plumbagin on silver nanoparticles imparts selectivity and sensitivity to plumbagin for targeted cancer cell apoptosis

Metallomics ◽  
2014 ◽  
Vol 6 (11) ◽  
pp. 2025-2033 ◽  
Author(s):  
N. Duraipandy ◽  
Rachita Lakra ◽  
Srivatsan Kunnavakkam Vinjimur ◽  
Debasis Samanta ◽  
Purna Sai K ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cancer Cell Apoptosis

Nano-caging of plumbagin for selective killing of cancer cells.

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