Hyperthermia potentiates cisplatin cytotoxicity and negative effects on mitochondrial functions in OVCAR-3 cells

Sukovas, Artūras; Šilkūnienė, Giedrė; Trumbeckaitė, Sonata; Jasukaitiene, Aldona; Degutytė-Fomins, Laima; Mildažienė, Vida; Gulbinas, Antanas; Banienė, Rasa; Dambrauskas, Žilvinas; Paškauskas, Saulius

doi:10.1007/s10863-019-09805-8

Cited by 8 publications

(7 citation statements)

References 37 publications

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“…MTT assay was performed by plating ESCs into 96-well tissue culture plates [16]. In general, 5000-10,000 ESCs per well were cultured for 48 h to reach full confluence and then treated with UV-B or G1.…”

Section: Cell Viabilitymentioning

confidence: 99%

Protective mechanism of GPR30 agonist G1 against ultraviolet B-induced injury in epidermal stem cells

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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The regeneration of the skin is vital to our wound healing and skin repair abilities. Adult epidermal stem cells (ESCs) have been shown to have the potential to renew old and dead skin cells, and ESCs have been implemented in stem cell-based therapies. GPR30 is a G protein-coupled membrane receptor for oestrogen, which has been shown to regulate cell proliferation and programmed cell death. Here, we examined the biological function of GPR30 in isolated adult murine ESCs. We show that GPR30 is fairly expressed in ESCs and is repressed upon ultraviolet B (UV-B) treatment in a dosedependent manner. The activation of GPR30 by its agonist G1 ameliorates UV-B induced cellular oxidative stress and induction of IL-6 and IL-8. Furthermore, G1 protects against UV-B-induced cell death and improves the viability of ESCs. G1 also suppresses UV-B-induced HMGB-1 expression and protects the capacity of ESCs from the harm by UV-B radiation. Mechanistically, we show that co-treatment with G1 rescues UV-B-induced reduced Wnt1, cyclin D1 and b-catenin production, indicating the involvement of conical Wnt/b-catenin. Collectively, our data indicate that the activation of GPR30 has a protective role in ESCs, and GPR30 agonist G1-mediated ESC protection has potential implications in stem cell-based therapies for skin diseases.

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Section: Cell Viabilitymentioning

confidence: 99%

Protective mechanism of GPR30 agonist G1 against ultraviolet B-induced injury in epidermal stem cells

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…All of the aforementioned problems have resulted in intense searches to increase the effectiveness of cisplatin, reduce its toxicity and overcome the mechanisms of cell resistance. Recent studies indicate that such methods may include combined therapy of cisplatin and hyperthermia or radiotherapy, as well as a combination of cisplatin with compounds of plant origin, and other drugs [17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Cisplatin in Ovarian Cancer Treatment—Known Limitations in Therapy Force New Solutions

Zoń

Bednarek

2023

IJMS

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Cisplatin is one of the most commonly used anticancer drugs worldwide. It is mainly used in the treatment of ovarian cancer, but also used in testicular, bladder and lung cancers. The significant advantage of this drug is the multidirectional mechanism of its anticancer action, with the most important direction being damaging the DNA of cancer cells. Unfortunately, cisplatin displays a number of serious disadvantages, including toxicity to the most important organs, such as kidneys, heart, liver and inner ear. Moreover, a significant problem among patients with ovarian cancer, treated with cisplatin, is the development of numerous resistance mechanisms during therapy, including changes in the processes of cellular drug import and export, changes in the DNA damage repair mechanisms, as well as numerous changes in the processes of apoptosis and autophagy. Due to all of the mentioned problems, strategies to increase the effectiveness of cisplatin in the treatment of ovarian cancer are intensively sought. The most important strategy includes the development of less toxic cisplatin analogs. Another important direction is combination therapy, involving the simultaneous use of cisplatin with different anticancer drugs, substances derived from plants, temperature or radiotherapy. Many years of observations accompanying the presence of cisplatin in the therapy made it possible to provide a series of verifiable, statistically significant data, but also to show how, over time, with the new information and scientific discoveries, it is possible to describe and understand the therapeutic problems observed in practice, such as the acquisition of drug resistance by tumor cells or induction of changes in the tumor microenvironment. According to the authors, confronting what we knew so far with what new trends offer has a profound meaning. This paper presents information on the history of cisplatin and describes the molecular mechanisms of its action and the development of resistance by cancer cells. In addition, our goal was to highlight a number of therapeutic strategies to increase the effectiveness of cisplatin in the treatment of ovarian cancer, as well as to identify methods to eliminate problems associated with the use of cisplatin.

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“…It has been demonstrated that hyperthermia potentiates the effect of cisplatin on tumor treatment by increasing cellular drug uptake and stimulating apoptosis [ 15 , 16 ]. It is well-known that gold nanoparticles (AuNP) can induce local hyperthermy by laser irradiation through a phenomenon known as surface plasmon resonance (SPR), which arises from coherent electron oscillation trough gold nanostructures’ surface [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

Gold Nanorods with Mesoporous Silica Shell: A Promising Platform for Cisplatin Delivery

et al. 2023

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The versatile combination of metal nanoparticles with chemotherapy agents makes designing multifunctional drug delivery systems attractive. In this work, we reported cisplatin’s encapsulation and release profile using a mesoporous silica-coated gold nanorods system. Gold nanorods were synthesized by an acidic seed-mediated method in the presence of cetyltrimethylammonium bromide surfactant, and the silica-coated state was obtained by modified Stöber method. The silica shell was modified first with 3-aminopropyltriethoxysilane and then with succinic anhydride to obtain carboxylates groups to improve cisplatin encapsulation. Gold nanorods with an aspect ratio of 3.2 and silica shell thickness of 14.74 nm were obtained, and infrared spectroscopy and ζ potential studies corroborated surface modification with carboxylates groups. On the other hand, cisplatin was encapsulated under optimal conditions with an efficiency of ~58%, and it was released in a controlled manner over 96 h. Furthermore, acidic pH promoted a faster release of 72% cisplatin encapsulated compared to 51% in neutral pH.

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Hyperthermia potentiates cisplatin cytotoxicity and negative effects on mitochondrial functions in OVCAR-3 cells

Cited by 8 publications

References 37 publications

Protective mechanism of GPR30 agonist G1 against ultraviolet B-induced injury in epidermal stem cells

Protective mechanism of GPR30 agonist G1 against ultraviolet B-induced injury in epidermal stem cells

Cisplatin in Ovarian Cancer Treatment—Known Limitations in Therapy Force New Solutions

Gold Nanorods with Mesoporous Silica Shell: A Promising Platform for Cisplatin Delivery

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