Induction of apoptosis in Jurkat cells by photoexcited psoralen derivatives: Implication of mitochondrial dysfunctions and caspases activation

Viola, Giampietro; Fortunato, Elena; Cecconet, Laura; Disarò, Silvia; Basso, Giuseppe

doi:10.1016/j.tiv.2006.09.016

Cited by 21 publications

(8 citation statements)

References 17 publications

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“…Cells were stained with propidium iodide (PI) and annexin-V-FITC (Prodotti Gianni) and cell death was measured by flow cytometry as the percentage annexin-V, PI-positive cells [25]. ROS production was assayed using dichlorodihydrofluorescein diacetate and flow cytometry as described [26].…”

Section: Methodsmentioning

confidence: 99%

Copper and bezafibrate cooperate to rescue cytochrome c oxidase deficiency in cells of patients with sco2 mutations

Casarin

Giorgi

Pertegato

et al. 2012

Orphanet J Rare Dis

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BackgroundMutations in SCO2 cause cytochrome c oxidase deficiency (COX) and a fatal infantile cardioencephalomyopathy. SCO2 encodes a protein involved in COX copper metabolism; supplementation with copper salts rescues the defect in patients’ cells. Bezafibrate (BZF), an approved hypolipidemic agent, ameliorates the COX deficiency in mice with mutations in COX10, another COX-assembly gene.MethodsWe have investigated the effect of BZF and copper in cells with SCO2 mutations using spectrophotometric methods to analyse respiratory chain activities and a luciferase assay to measure ATP production..ResultsIndividual mitochondrial enzymes displayed different responses to BZF. COX activity increased by about 40% above basal levels (both in controls and patients), with SCO2 cells reaching 75-80% COX activity compared to untreated controls. The increase in COX was paralleled by an increase in ATP production. The effect was dose-dependent: it was negligible with 100 μM BZF, and peaked at 400 μM BZF. Higher BZF concentrations were associated with a relative decline of COX activity, indicating that the therapeutic range of this drug is very narrow. Combined treatment with 100 μM CuCl2 and 200 μM BZF (which are only marginally effective when administered individually) achieved complete rescue of COX activity in SCO2 cells.ConclusionsThese data are crucial to design therapeutic trials for this otherwise fatal disorder. The additive effect of copper and BZF will allow to employ lower doses of each drug and to reduce their potential toxic effects. The exact mechanism of action of BZF remains to be determined.

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Section: Methodsmentioning

confidence: 99%

Copper and bezafibrate cooperate to rescue cytochrome c oxidase deficiency in cells of patients with sco2 mutations

Casarin

Giorgi

Pertegato

et al. 2012

Orphanet J Rare Dis

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“…PUVA therapy (photoactivated psoralens) is beneficial for patients with vitiligo, psoriasis, and skin diseases. PUVA activates caspase-3, -8 and -9 in Jurkat (human tumor T-cell line) [127]. PUVA, the photoactivated psoralens (5-MOP and 8-MOP) induce apoptosis in MCF-7, ZR-75 and SKBR-3 by caspase and p53 upregulation, PI3K/AKT downregulation and effective against breast hormone-responsive cancers [128].…”

Section: Furanocoumarins and Cancer Risksmentioning

confidence: 99%

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Ahmed

Khan

Aschner

et al. 2020

IJMS

128

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Cancer is one of the most extreme medical conditions in both developing and developed countries around the world, causing millions of deaths each year. Chemotherapy and/or radiotherapy are key for treatment approaches, but both have numerous adverse health effects. Furthermore, the resistance of cancerous cells to anticancer medication leads to treatment failure. The rising burden of cancer overall requires novel efficacious treatment modalities. Natural medications offer feasible alternative options against malignancy in contrast to western medication. Furanocoumarins’ defensive and restorative impacts have been observed in leukemia, glioma, breast, lung, renal, liver, colon, cervical, ovarian, and prostate malignancies. Experimental findings have shown that furanocoumarins activate multiple signaling pathways, leading to apoptosis, autophagy, antioxidant, antimetastatic, and cell cycle arrest in malignant cells. Additionally, furanocoumarins have been shown to have chemo preventive and chemotherapeutic synergistic potential when used in combination with other anticancer drugs. Here, we address different pathways which are activated by furanocoumarins and their therapeutic efficacy in various tumors. Ideally, this review will trigger interest in furanocoumarins and their potential efficacy and safety as a cancer lessening agents.

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“…20,21,28,29 During apoptosis membrane blebbing, chromatin condensation, DNA fragmentation, formation of apoptotic bodies, and activation of caspases can be observed. [30][31][32][33][34][35] Mitochondrial dysfunction is involved in caspase activation, [36][37][38] and proteins of the Bcl2 family (Bax and Bcl2) that are localized in the mitochondria suggest their role in the regulation of mitochondria-mediated apoptosis. [30][31][32][33][34][35] Furthermore, nitric oxide (NO), a potent signaling molecule contributes to mitochondrial dysfunction by inhibiting cytochrome c oxidase, resulting in overproduction of reactive superoxide species.…”

Section: Introductionmentioning

confidence: 99%

Prolonged exposure of resveratrol induces reactive superoxide species–independent apoptosis in murine prostate cells

et al. 2017

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Nitric oxide, a signaling molecule, inhibits mitochondrial respiration by binding with cytochrome c oxidase, resulting in elevated production of reactive superoxide species (reactive oxygen and nitrogen) in the mitochondria and increased susceptibility to cell death. Generation of mitochondrial superoxide species can be suppressed by natural compounds such as resveratrol, a dietary polyphenol found in the skin of red fruits. In various cancer cells, resveratrol shows anti-oxidant and cancer preventive properties. Since, the effect of resveratrol on reactive superoxide species-independent apoptosis in prostate cancer cells is not well illustrated; therefore, we investigated this phenomenon in TRAMP murine prostate cancer cells. To accomplish this, TRAMP cells were incubated with resveratrol, resveratrol + DETA-NONOate, DETA-NONOate (nitric oxide donor), resveratrol + L-NMMA, or L-NMMA (nitric oxide inhibitor) for 48 h, and reactive superoxide species in the mitochondria and culture supernatant were measured. In addition, the mitochondrial membrane potential, cell viability, expression of apoptotic markers (Bax and Bcl2), γ-H2A.x, p53, and caspase-3 was determined. We found that resveratrol suppressed reactive superoxide species such as reactive oxygen species in the mitochondria and nitric oxide in culture supernatant when compared to the DETA-NONOate treatment and disrupted the mitochondrial membrane potential. Resveratrol also reduced cell viability, altered the expression of apoptotic markers (Bax and Bcl2), and increased expression of γ-H2A.x (indicative marker of DNA fragmentation) and p53 (a critical DNA damage response protein). However, there was no appreciable modulation of the caspase-3. Therefore, our data suggest that resveratrol induces superoxide species-independent apoptosis and may act as a therapeutic agent against prostate cancer.

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Induction of apoptosis in Jurkat cells by photoexcited psoralen derivatives: Implication of mitochondrial dysfunctions and caspases activation

Cited by 21 publications

References 17 publications

Copper and bezafibrate cooperate to rescue cytochrome c oxidase deficiency in cells of patients with sco2 mutations

Copper and bezafibrate cooperate to rescue cytochrome c oxidase deficiency in cells of patients with sco2 mutations

Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic Aspects

Prolonged exposure of resveratrol induces reactive superoxide species–independent apoptosis in murine prostate cells

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