scholarly journals Comprehensive identification of genes driven by ERV9-LTRs reveals TNFRSF10B as a re-activatable mediator of testicular cancer cell death

2015 ◽  
Vol 23 (1) ◽  
pp. 64-75 ◽  
Author(s):  
U Beyer ◽  
S K Krönung ◽  
A Leha ◽  
L Walter ◽  
M Dobbelstein
Keyword(s):  
Cell Death ◽  
Testicular Cancer ◽  
Cancer Cell ◽  
Cancer Cell Death

New Insight into 2-Methoxyestradiol- a Possible Physiological Link between Neurodegeneration and Cancer Cell Death

2016 ◽  
Vol 23 (15) ◽  
pp. 1513-1527 ◽  
Author(s):  
Magdalena Gorska ◽  
Alicja Kuban-Jankowska ◽  
Jaroslaw Slawek ◽  
Michal Wozniak
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Cancer Cell Death ◽  
Insight Into

Zinc chelator TPEN induces pancreatic cancer cell death through causing oxidative stress and inhibiting cell autophagy

2019 ◽  
Vol 234 (11) ◽  
pp. 20648-20661 ◽  
Author(s):  
Zhen Yu ◽  
Ze Yu ◽  
ZhenBao Chen ◽  
Lin Yang ◽  
MingJun Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Death ◽  
Zinc Chelator

Magneto Mitochondrial Dysfunction Mediated Cancer Cell Death Using Intracellular Magnetic Nano-Transducers

2021 ◽  
Author(s):  
Wooram Park ◽  
Seok-Jo Kim ◽  
Paul Cheresh ◽  
Jeanho Yun ◽  
Byeongdu Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Sensitivity ◽  
Intrinsic Pathway ◽  
Cancer Cell Death

Mitochondria are crucial regulators of the intrinsic pathway of cancer cell death. The high sensitivity of cancer cells to mitochondrial dysfunction offers opportunities for emerging targets in cancer therapy. Herein,...

scholarly journals Correction to Inducing Cancer Cell Death by Targeting Its Nucleus: Solid Gold Nanospheres versus Hollow Gold Nanocages

2013 ◽  
Vol 24 (8) ◽  
pp. 1414-1414 ◽  
Author(s):  
Megan A. Mackey ◽  
Farhat Saira ◽  
Mahmoud A. Mahmoud ◽  
Mostafa A. El-Sayed
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Gold Nanospheres ◽  
Solid Gold ◽  
Cancer Cell Death ◽  
Gold Nanocages

scholarly journals Membrane-Interacting DNA Nanotubes Induce Cancer Cell Death

Nanomaterials ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2003
Author(s):  
Samet Kocabey ◽  
Aslihan Ekim Kocabey ◽  
Roger Schneiter ◽  
Curzio Rüegg
Keyword(s):  
Drug Delivery ◽  
Cell Death ◽  
Cytochrome C ◽  
Membrane Permeability ◽  
Cancer Cell ◽  
Cell Membrane Permeability ◽  
Caspase Activity ◽  
Cancer Cell Death ◽  
Modified Dna ◽  
Dna Nanotubes

DNA nanotechnology offers to build nanoscale structures with defined chemistries to precisely position biomolecules or drugs for selective cell targeting and drug delivery. Owing to the negatively charged nature of DNA, for delivery purposes, DNA is frequently conjugated with hydrophobic moieties, positively charged polymers/peptides and cell surface receptor-recognizing molecules or antibodies. Here, we designed and assembled cholesterol-modified DNA nanotubes to interact with cancer cells and conjugated them with cytochrome c to induce cancer cell apoptosis. By flow cytometry and confocal microscopy, we observed that DNA nanotubes efficiently bound to the plasma membrane as a function of the number of conjugated cholesterol moieties. The complex was taken up by the cells and localized to the endosomal compartment. Cholesterol-modified DNA nanotubes, but not unmodified ones, increased membrane permeability, caspase activation and cell death. Irreversible inhibition of caspase activity with a caspase inhibitor, however, only partially prevented cell death. Cytochrome c-conjugated DNA nanotubes were also efficiently taken up but did not increase the rate of cell death. These results demonstrate that cholesterol-modified DNA nanotubes induce cancer cell death associated with increased cell membrane permeability and are only partially dependent on caspase activity, consistent with a combined form of apoptotic and necrotic cell death. DNA nanotubes may be further developed as primary cytotoxic agents, or drug delivery vehicles, through cholesterol-mediated cellular membrane interactions and uptake.

scholarly journals The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Wenwen Tang ◽  
Shaomi Zhu ◽  
Xin Liang ◽  
Chi Liu ◽  
Linjiang Song
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Causes Of Death ◽  
Vital Role ◽  
Cancer Cell Proliferation ◽  
Biological Targets ◽  
Cancer Cell Death ◽  
Different Types ◽  
Non Coding Rnas ◽  
Tumor Death

With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.

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