Silver nanoparticles potentiate antitumor and oxidant actions of cisplatin via the stimulation of TRPM2 channel in glioblastoma tumor cells

Akyuva, Yener; Nazıroğlu, Mustafa

doi:10.1016/j.cbi.2022.110261

Cited by 10 publications

(21 citation statements)

References 46 publications

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“…represent an effective alternative antitumor strategy to current systemic treatments (Akyuva & Nazıroğlu, 2023;Kaya et al, 2023;Nur et al, 2017). In addition, the chemotherapeutic agents have several harmful side effects on prognosis, quality of life, and waste of health care resources in patients with cancer, although the antioxidants have no adverse action during the killing of cancer cells (Tasdogan et al, 2021).…”

Section: Cell Ell B Biology Iology I International Nternationalmentioning

confidence: 99%

“…Recently, it was reported that the treatment of SiNPs induced synergic action against several cisplatin-resistant tumor cell lines through the activation of CASP3, CASP8, and CASP9. SiNPs (Akyuva & Nazıroğlu, 2023) and 5-FU may operate synergistically to inhibit HT-29 cells because of their different actions on the control of Ca ). In the remaining analyses, the 2 × 10 6 cells were seeded in T25 cm 2 flasks with filter caps.…”

Section: Cell Ell B Biology Iology I International Nternationalmentioning

confidence: 99%

“…was used (Akyuva & Nazıroğlu, 2023;Nur et al, 2017). In the assay, a pink-colored dye at the stage of the phosphatidylserine transmembrane movement was taken by the apoptotic cells, and its uptake occurred simultaneously until blebbing occurred.…”

Section: Assays Of Apoptosis Casp3 Casp8 and Casp9mentioning

confidence: 99%

“…The activities of CASP3, CASP8, and CASP9 were assayed as previously reported with minor modifications (Akyuva & Nazıroğlu, 2023).…”

Section: Assays Of Apoptosis Casp3 Casp8 and Casp9mentioning

confidence: 99%

“…Under laser stimulation, the propidium iodide (PI) dye accumulates in the nucleus of injured cells and represents the ret image. The cells in the dishes were treated with PI (4 μM/mL) and Hoechst 33342 (4 μM/mL) (Cell Signaling Technology) for 15-20 min before capturing the red/blue (PI/Hoechst) pictures in the LSM-800 analyses (objective: 40× oil) (Akyuva & Nazıroğlu, 2023). After washing the cells with extracellular buffer, the diode laser was used to stimulate PI at 561 nm, while the laser was used to stimulate Hoechst 33342 at 405 nm.…”

Section: Cell Death Rate Assaysmentioning

confidence: 99%

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Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Kaya

2024

Cell Biology International

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The involvement of the TRP vanilloid 1 (TRPV1) cation channel on the 5‐Fluorouracil (5‐FU)‐caused Ca2+ signals through the activation of the apoptotic signaling pathway and stimulating the mitochondrial Ca2+ and Zn2+ accumulation‐induced reactive oxygen species (ROS) productions in several cancer cells, except the colorectal cancer (HT‐29) cell line, was recently reported. I aimed to investigate the action of silver nanoparticles (SiNPs) and 5‐FU incubations through the activation of TRPV1 on ROS, apoptosis, and cell death in the HT‐29 cell line. The cells were divided into four groups: control, SiNP (100 µM for 48 h), 5‐FU (25 μM for 24 h), and 5‐FU + SiNP. SiNP treatment through TRPV1 activation (via capsaicin) stimulated the oxidant and apoptotic actions of 5‐FU in the cells, whereas they were diminished in the cells by the TRPV1 antagonist (capsazepine) treatment. The apoptotic and cell death actions of 5‐FU were determined by increasing the propidium iodide/Hoechst rate, caspase‐3, ‐8, and ‐9 activations, mitochondrial membrane depolarization, lipid peroxidation, and ROS, but decreasing the glutathione and glutathione peroxidase. The increase of cytosolic free Ca2+ and Zn2+ into mitochondria via the stimulation of TRPV1 current density increased oxidant and apoptotic properties of 5‐FU in the cells. For the therapy of HT‐29 tumor cells, I found that the combination of SiNPs and 5‐FU was synergistic via TRPV1 activation.

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Section: Cell Ell B Biology Iology I International Nternationalmentioning

confidence: 99%

Section: Cell Ell B Biology Iology I International Nternationalmentioning

confidence: 99%

Section: Assays Of Apoptosis Casp3 Casp8 and Casp9mentioning

confidence: 99%

“…The activities of CASP3, CASP8, and CASP9 were assayed as previously reported with minor modifications (Akyuva & Nazıroğlu, 2023).…”

Section: Assays Of Apoptosis Casp3 Casp8 and Casp9mentioning

confidence: 99%

Section: Cell Death Rate Assaysmentioning

confidence: 99%

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Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Kaya

2024

Cell Biology International

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Nanocarriers for the treatment of glioblastoma multiforme: A succinct review of conventional and repositioned drugs in the last decade

Bayoumi,

Youshia,

Arafa

et al. 2024

Archiv der Pharmazie

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Glioblastoma multiforme is a very combative and threatening type of cancer. The standard course of treatment involves excising the tumor surgically, then administering chemotherapy and radiation therapy. Because of the presence of the blood–brain barrier and the unique characteristics of the tumor microenvironment, chemotherapy is extremely difficult and has a high incidence of relapse. With their capacity to precisely target and transport therapeutic medications to the tumor while overcoming the challenges provided by invasive and infiltrative gliomas, nanocarriers offer a potentially beneficial treatment option for gliomas. Drug repositioning or, in other words, finding novel therapeutic uses for medications that have received approval for previous uses has also recently emerged to provide alternative treatments for many diseases, with glioblastoma being among them. In this article, our goal is to shed light on the pathogenesis of glioma and summarize the proposed treatment approaches in the last decade, highlighting how combining repositioned drugs and nanocarriers technology can reduce drug resistance and improve therapeutic efficacy in primary glioma.

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Erucic acid increases the potency of cisplatin‐induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

Nazıroğlu,

Çarhan,

Nazıroğlu

2024

Cell Biology International

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Erucic acid (ErA) is a source of omega‐9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT‐29 human colorectal cancer cell line. The apoptotic and Ca2+ signaling pathways in tumor cells are triggered when mitochondrial Ca2+ and Zn2+ accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2. ErA‐induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin (CSP). We aimed to study the effects of ErA and CSP incubations on ROS, apoptosis, and cell death in the HT‐29 cells by activating TRPM2. The cells were divided into five groups: control, ErA (200 µM for 48 h), CSP (25 µM for 24 h), and ErA + CSP + TRPM2 antagonists (200 µM carvacrol and 25 µM N‐(p‐amylcinnamoyl)anthranilic acid for 24 h). The TRPM2 antagonists reduced ErA plus CSP‐induced increases in H2O2‐induced intracellular free Ca2+ concentration ([Ca2+]c) and adenosine diphosphate‐ribose‐caused TRPM2 currents. ErA and CSP were found to cause apoptosis and cell death by raising the intracellular free Zn2+ concentration (Zn2+]c), caspase‐3, −8, and −9, mitochondrial membrane dysfunction, and ROS, while lowering reduced glutathione, cell viability, and cell number. The oxidative, apoptotic, and tumor cell death effects of CSP in the cells were enhanced by the increase of ErA‐mediated [Ca2+]c and Zn2+]c entering mitochondria through the activation of TRPM2. In conclusion, we observed that the combination of ErA and CSP was synergistic via TRPM2 activation for the treatment of HT‐29 tumor cells.

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Silver nanoparticles potentiate antitumor and oxidant actions of cisplatin via the stimulation of TRPM2 channel in glioblastoma tumor cells

Cited by 10 publications

References 46 publications

Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Nanocarriers for the treatment of glioblastoma multiforme: A succinct review of conventional and repositioned drugs in the last decade

Erucic acid increases the potency of cisplatin‐induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

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