scholarly journals Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

Author(s):  
Shuang Wu ◽  
Tianye Li ◽  
Weiwei Liu ◽  
Yongye Huang

Cell death induction has become popular as a novel cancer treatment. Ferroptosis, a newly discovered form of cell death, features regulated, iron-dependent accumulation of lipid hydroperoxides. Since this word “ferroptosis” was coined, numerous studies have examined the complex relationship between ferroptosis and cancer. Here, starting from the intrinsic hallmarks of cancer and cell death, we discuss the theoretical basis of cell death induction as a cancer treatment. We review various aspects of the relationship between ferroptosis and cancer, including the genetic basis, epigenetic modification, cancer stem cells, and the tumor microenvironment, to provide information and support for further research on ferroptosis. We also note that exosomes can be applied in ferroptosis-based therapy. These extracellular vesicles can deliver different molecules to modulate cancer cells and cell death pathways. Using exosomes to control ferroptosis occurring in targeted cells is promising for cancer therapy.

2021 ◽  
Vol 11 ◽  
Author(s):  
Dengqiang Wu ◽  
Changhong Wei ◽  
Yujie Li ◽  
Xuejia Yang ◽  
Sufang Zhou

The way of cell death can be roughly divided into two categories: cell necrosis and PCD(programmed cell death). Pyroptosis is a kind of PCD, its occurrence depends on the gasdermin protein family and it will produce inflammatory response. With constant research in recent years, more and more evidences show that pyroptosis is closely related to the occurrence and development of tumors. The treatment of tumors is a big problem worldwide. We focus on whether we can discover new potential tumor markers and new therapeutic targets from the mechanism. If we can understand the mechanism of pyroptosis and clear the relationship between pyroptosis and the development of tumors, this may provide a new reference for clinical cancer treatment.


2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Melissa S. Phuong ◽  
Rafael E. Hernandez ◽  
Daniel J. Wolter ◽  
Lucas R. Hoffman ◽  
Subash Sad

AbstractPseudomonas aeruginosa is a common respiratory pathogen in cystic fibrosis (CF) patients which undergoes adaptations during chronic infection towards reduced virulence, which can facilitate bacterial evasion of killing by host cells. However, inflammatory cytokines are often found to be elevated in CF patients, and it is unknown how chronic P. aeruginosa infection can be paradoxically associated with both diminished virulence in vitro and increased inflammation and disease progression. Thus, we investigated the relationship between the stimulation of inflammatory cell death pathways by CF P. aeruginosa respiratory isolates and the expression of key inflammatory cytokines. We show that early respiratory isolates of P. aeruginosa from CF patients potently induce inflammasome signaling, cell death, and expression of IL-1β by macrophages, yet little expression of other inflammatory cytokines (TNF, IL-6 and IL-8). In contrast, chronic P. aeruginosa isolates induce relatively poor macrophage inflammasome signaling, cell death, and IL-1β expression but paradoxically excessive production of TNF, IL-6 and IL-8 compared to early P. aeruginosa isolates. Using various mutants of P. aeruginosa, we show that the premature cell death of macrophages caused by virulent bacteria compromises their ability to express cytokines. Contrary to the belief that chronic P. aeruginosa isolates are less pathogenic, we reveal that infections with chronic P. aeruginosa isolates result in increased cytokine induction due to their failure to induce immune cell death, which results in a relatively intense inflammation compared with early isolates.


2013 ◽  
Vol 41 (2) ◽  
pp. 657-663 ◽  
Author(s):  
Colin R. Lenihan ◽  
Cormac T. Taylor

Hypoxia is a frequently encountered feature of the cellular microenvironment in a number of pathophysiological processes in which programmed cell death (apoptosis) affects disease progression including, but not limited to, cancer, chronic inflammation, myocardial infarction, stroke and ischaemic acute kidney injury. In these diseases, the presence of hypoxia can significantly affect the rate of cell death and thus may make a significant contribution to disease progression. In the present review, we discuss the complex relationship that exists between the presence of hypoxia and the regulation of cell death pathways.


1993 ◽  
Vol 2 (3) ◽  
pp. 52-55 ◽  
Author(s):  
Michael Collins ◽  
Robert McDonald ◽  
Robert Stanley ◽  
Timothy Donovan ◽  
C. Frank Bonebrake

This report describes an unusual and persistent dysphonia in two young women who had taken a therapeutic regimen of isotretinoin for intractable acne. We report perceptual and instrumental data for their dysphonia, and pose a theoretical basis for the relationship of dysphonia to this drug. We also provide recommendations for reducing the risk of acquiring a dysphonia during the course of treatment with isotretinoin.


2020 ◽  
Vol 48 (3) ◽  
pp. 137-152
Author(s):  
Marko Manevski ◽  
Dinesh Devadoss ◽  
Ruben Castro ◽  
Lauren Delatorre ◽  
Adriana Yndart ◽  
...  

Author(s):  
V. Tusheva

The determinants of value orientations of a teacher of higher artistic education are identified, qualitative and instrumental properties of a teacher’s consciousness are determined, the relationship between value and sense-bearing processes at the level of cultural and personal senses and outlook priorities correlated with the main messages of postnonclassical science are revealed in the article on the bases of humanistic personally oriented paradigm. Different vectors of deployment of consciousness (self-consciousness) as a teacher’s personal formation in artistic education are considered, the positions which lay the theoretical basis for the development of value and sense-oriented learning, its multicultural, pedagogical and individual-personal contexts are formulated.


2020 ◽  
Vol 27 ◽  
Author(s):  
Xinrui Li ◽  
Liang Ma ◽  
Ping Fu

: Mitochondria are potent source of cellular reactive oxygen species (ROS) and are vulnerable to oxidative damage. Mitochondria dysfunction could result in adenosine triphosphate (ATP) decrease and cell death. The kidney is an ATPconsuming organ, and the relationship between mitochondrial dysfunction and renal disease has been long noted. Mitochondrial targeting is a novel strategy for kidney diseases. At present, there are several ways to target mitochondria such as the addition of a triphenylphosphonium cation, mitochondria-targeted peptides, and nanocarrier. There are also a variety of choices for the payload, such as nitroxides, quinone derivates, vitamins and so on. This review summarized chemical and also clinical characteristics of various mitochondria-targeted antioxidants and focused on their application and perspectives in kidney diseases.


Author(s):  
Nivedita Bhardwaj ◽  
Nancy Tripathi ◽  
Bharat Goel ◽  
Shreyans K. Jain

: During cancer progression, the unrestricted proliferation of cells is supported by the impaired cell death response provoked by certain oncogenes. Both autophagy and apoptosis are the signaling pathways of cell death, which are targeted for cancer treatment. Defects in apoptosis result in reduced cell death and ultimately tumor progression. The tumor cells lacking apoptosis phenomena are killed by ROS- mediated autophagy. The autophagic programmed cell death requires apoptosis protein for inhibiting tumor growth; thus, the interconnection between these two pathways determines the fate of a cell. The cross-regulation of autophagy and apoptosis is an important aspect to modulate autophagy, apoptosis and to sensibilise apoptosis-resistant tumor cells under metabolic stress and might be a rational approach for drug designing strategy for the treatment of cancer. Numerous proteins involved in autophagy have been investigated as the druggable target for anticancer therapy. Several compounds of natural origin have been reported, to control autophagy activity through the PI3K/Akt/mTOR key pathway. Diosgenin, a steroidal sapogenin has emerged as a potential candidate for cancer treatment. It induces ROS-mediated autophagy, inhibits PI3K/Akt/mTOR pathway, and produces cytotoxicity selectively in cancer cells. This review aims to focus on optimal strategies using diosgenin to induce apoptosis by modulating the pathways involved in autophagy regulation and its potential implication in the treatment of various cancer. The discussion has been extended to the medicinal chemistry of semi-synthetic derivatives of diosgenin exhibiting anticancer activity.


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