scholarly journals Remotely Activated Nanoparticles for Anticancer Therapy

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Luisa Racca ◽  
Valentina Cauda

AbstractCancer has nowadays become one of the leading causes of death worldwide. Conventional anticancer approaches are associated with different limitations. Therefore, innovative methodologies are being investigated, and several researchers propose the use of remotely activated nanoparticles to trigger cancer cell death. The idea is to conjugate two different components, i.e., an external physical input and nanoparticles. Both are given in a harmless dose that once combined together act synergistically to therapeutically treat the cell or tissue of interest, thus also limiting the negative outcomes for the surrounding tissues. Tuning both the properties of the nanomaterial and the involved triggering stimulus, it is possible furthermore to achieve not only a therapeutic effect, but also a powerful platform for imaging at the same time, obtaining a nano-theranostic application. In the present review, we highlight the role of nanoparticles as therapeutic or theranostic tools, thus excluding the cases where a molecular drug is activated. We thus present many examples where the highly cytotoxic power only derives from the active interaction between different physical inputs and nanoparticles. We perform a special focus on mechanical waves responding nanoparticles, in which remotely activated nanoparticles directly become therapeutic agents without the need of the administration of chemotherapeutics or sonosensitizing drugs.

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Wenwen Tang ◽  
Shaomi Zhu ◽  
Xin Liang ◽  
Chi Liu ◽  
Linjiang Song

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.


Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2330
Author(s):  
Charlotta Bengtson ◽  
Annemie Bogaerts

Cold atmospheric plasma (CAP) is a promising new agent for (selective) cancer treatment, but the underlying cause of the anti-cancer effect of CAP is not well understood yet. Among different theories and observations, one theory in particular has been postulated in great detail and consists of a very complex network of reactions that are claimed to account for the anti-cancer effect of CAP. Here, the key concept is a reactivation of two specific apoptotic cell signaling pathways through catalase inactivation caused by CAP. Thus, it is postulated that the anti-cancer effect of CAP is due to its ability to inactivate catalase, either directly or indirectly. A theoretical investigation of the proposed theory, especially the role of catalase inactivation, can contribute to the understanding of the underlying cause of the anti-cancer effect of CAP. In the present study, we develop a mathematical model to analyze the proposed catalase-dependent anti-cancer effect of CAP. Our results show that a catalase-dependent reactivation of the two apoptotic pathways of interest is unlikely to contribute to the observed anti-cancer effect of CAP. Thus, we believe that other theories of the underlying cause should be considered and evaluated to gain knowledge about the principles of CAP-induced cancer cell death.


2006 ◽  
Vol 290 (1) ◽  
pp. F4-F13 ◽  
Author(s):  
Neil G. Docherty ◽  
Orfhlaith E. O'Sullivan ◽  
Declan A. Healy ◽  
John M. Fitzpatrick ◽  
R. William G. Watson

Ureteric obstruction is frequently encountered in primary care urology and can lead to damage to the ipsilateral kidney. Relief of all types of obstruction generally leads to the normalization of any deterioration in renal function noted at diagnosis. However, some evidence from animal models suggests that obstruction can cause progressive deleterious effects on renal function and blood pressure control, especially in the presence of preexisting pathologies such as essential hypertension. The last 10 years have seen a proliferation of studies in rodents wherein complete unilateral ureteric obstruction has been used as a model of renal fibrosis. However, the relevance of the findings to human obstructive uropathy has, in many cases, not been the primary aim. In this review, we outline the major events linking damage to the renal parenchyma and cell death to the evolution of fibrosis following obstruction. Special focus is given to the role of apoptosis as a major cause of cell death during and post-complete ureteric obstruction. Several interventions that reduce tubular apoptosis are discussed in terms of their ability to prevent subsequent progression to end-organ damage and fibrosis.


2013 ◽  
Vol 56 (12) ◽  
pp. 4823-4839 ◽  
Author(s):  
Alexander Kornienko ◽  
Véronique Mathieu ◽  
Shiva K. Rastogi ◽  
Florence Lefranc ◽  
Robert Kiss

2013 ◽  
Vol 42 (4) ◽  
pp. 1417-1426 ◽  
Author(s):  
YUMIN LI ◽  
JUNQIANG ZHANG ◽  
HAIZHEN MA ◽  
XIAOHUI CHEN ◽  
TAO LIU ◽  
...  

Author(s):  
Yifei Le ◽  
Zhijie Zhang ◽  
Cui Wang ◽  
Dezhao Lu

Background: Cell death is a fundamental biological phenomenon that contributes to the pathogenesis of various diseases. Regulation of iron and iron metabolism has received considerable research interests especially concerning the progression of metabolic diseases. Discussion: Emerging evidence shows that ferroptosis, a non-apoptotic programmed cell death induced by iron-dependent lipid peroxidation, contributes to the development of complex diseases such as non-alcoholic steatohepatitis, cardiomyopathy, renal ischemia-reperfusion, and neurodegenerative diseases. Therefore, inhibiting ferroptosis can improve the pathophysiology of associated metabolic diseases. This review describes the vital role of ferroptosis in mediating the development of certain metabolic diseases. Besides, the potential risk of iron and ferroptosis in atherosclerosis and cardiovascular diseases is also described. Iron overload and ferroptosis are potential secondary causes of death in metabolic diseases. Moreover, this review also provides potential novel approaches against ferroptosis based on recent research advances. Conclusion: Several controversies exist concerning mechanisms underlying ferroptotic cell death in metabolic diseases, particularly in atherosclerosis. Since ferroptosis participates in the progression of metabolic diseases such as non-alcoholic steatohepatitis (NASH), there is a need to develop new drugs targeting ferroptosis to alleviate such diseases.


Author(s):  
Rajkumar Venkatadri ◽  
Clayton Wright ◽  
Vivek Kaushik ◽  
Yogesh Kulkarni ◽  
Juan Sebastian Yakisich ◽  
...  

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