Ciprofloxacin-mediated induction of S-phase cell cycle arrest and apoptosis in COLO829 melanoma cells

Beberok, Artur; Wrześniok, Dorota; Minecka, Aldona; Rok, Jakub; Delijewski, Marcin; Rzepka, Zuzanna; Respondek, Michalina; Buszman, Ewa

doi:10.1016/j.pharep.2017.07.007

Cited by 53 publications

(42 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The highest concentration of ciprofloxacin (1.0 mM) induced oligonucleosomal DNA fragmentation (the presence of sub-G 1 fraction), strongly suggesting that apoptosis was induced via the p53-dependent pathway. These results are consistent with the results of our recent study, which revealed that ciprofloxacin mediates the induction of S-phase arrest and apoptosis in COLO829 melanoma cells (41). They are also consistent with the results of study by Yadav et al (13), which identified the ability of ciprofloxacin to induce DNA fragmentation and S-phase arrest in human pancreatic cancer cells.…”

Section: Discussionsupporting

confidence: 93%

Ciprofloxacin triggers the apoptosis of human triple-negative breast cancer MDA-MB-231 cells via the p53/Bax/Bcl-2 signaling pathway

et al. 2018

Self Cite

View full text Add to dashboard Cite

Fluoroquinolone antibiotics induce cytotoxicity in various cancer cell lines and may therefore represent a potentially important source of novel anticancer agents. The aim of the present study was to examine the effect of ciprofloxacin on the viability, redox balance, apoptosis, expression of p53, Bax and Bcl-2, cell cycle distribution and DNA fragmentation of triple-negative MDA-MB-231 breast cancer cells. The results of the present study demonstrated that ciprofloxacin decreases cell viability in a dose- and time-dependent manner. The half maximal inhibitory concentration values of ciprofloxacin in MDA-MB-231 cells following treatment for 24, 48 and 72 h were 0.83, 0.14 and 0.03 µmol/ml, respectively. Furthermore, it was demonstrated that ciprofloxacin altered the redox signaling pathway, as determined by intracellular glutathione depletion. The results of Annexin V/propidium iodide staining revealed that ciprofloxacin triggered the apoptosis of MDA-MB-231 cells. Furthermore, cipfloxacin treatment stimulated the loss of the mitochondrial transmembrane potential via the Bax/Bcl-2-dependent pathway, thus inducing apoptosis. Ciprofloxacin induced cell cycle arrest at the S-phase; therefore it was hypothesized that ciprofloxacin inhibits topoisomerase II. Oligonucleosomal DNA fragmentation and the elevation of p53 expression were observed in the present study, indicating that this late-apoptotic event may be mediated by the p53-dependent pathway. Therefore, the results of the current study provide important molecular data concerning the cellular cascade, which may explain the cytotoxicity induced by ciprofloxacin in human triple-negative breast cancer cells, thus providing a novel insight into the therapeutic properties of this drug.

show abstract

Section: Discussionsupporting

confidence: 93%

Ciprofloxacin triggers the apoptosis of human triple-negative breast cancer MDA-MB-231 cells via the p53/Bax/Bcl-2 signaling pathway

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…The anticancer activity of Ciprofloxacin has been demonstrated in human and animal cancer cell lines in vitro, such as human bladder cancer cell lines, human colorectal cell lines, hamster ovarian cancer cell lines, and human hepatocellular carcinoma [33,34]. Artur Beberok and Dorota Wrzesniok et al have shown that the incubation period would be extended to 48 h and 72 h in low concentration (0.01 mM and 0.1 mM) of ciprofloxacin, and that melanoma cells would appear stagnation of S phase of the cycle by cell fluorescence image analysis through mechanisms associated with topoisomerase II inhibition [33,34]. In contrast, Kloskowski et al demonstrated that ciprofloxacin caused cell stagnation at the G2/M checkpoint in human non-small cell lung cancer [35].…”

Section: Ciprofloxacinmentioning

confidence: 99%

Antibiotics for cancer treatment: A double-edged sword

et al. 2020

View full text Add to dashboard Cite

Various antibiotics have been used in the treatment of cancers, via their anti-proliferative, pro-apoptotic and anti-epithelial-mesenchymal-transition (EMT) capabilities. However, increasingly studies have indicated that antibiotics may also induce cancer generation by disrupting intestinal microbiota, which further promotes chronic inflammation, alters normal tissue metabolism, leads to genotoxicity and weakens the immune response to bacterial malnutrition, thereby adversely impacting cancer treatment. Despite the advent of high-throughput sequencing technology in recent years, the potential adverse effects of antibiotics on cancer treatments via causing microbial imbalance has been largely ignored. In this review, we discuss the double-edged sword of antibiotics in the field of cancer treatments, explore their potential mechanisms and provide solutions to reduce the potential negative effects of antibiotics.

show abstract

“…Cell cycle phase distribution of astrocytes after the 27 day culture in medium with/without (OH)Cbl(c-lactam) was analyzed following a previously described method [21]. In brief, cells were fixed with ice-cold 70% ethanol at 4 • C for 24 h, stained with Solution 3 for 5 min at 37 • C, and then analyzed using the image cytometer with the adequate protocol-Cell Cycle Analysis of Fixed Cells or DNA Fragmentation Assay (ChemoMetec).…”

Section: Cell Cycle Assay and Dna Fragmentation Assaymentioning

confidence: 99%

“…Astrocytes at day 27 of culture with/without (OH)Cbl(c-lactam) were examined in terms of the mitochondrial transmembrane potential (∆Ψ m ). The analysis was performed using the image cytometer NucleoCounter NC-3000 following JC-1/DAPI staining according to a previously described method [21].…”

Section: Mitochondrial Potential Assaymentioning

confidence: 99%

Cobalamin Deficiency: Effect on Homeostasis of Cultured Human Astrocytes

Rzepka

Rok

Respondek

et al. 2019

Cells

Self Cite

View full text Add to dashboard Cite

Cobalamin deficiency is an important health problem. The major non-hematological symptoms of hypocobalaminemia are nervous system disorders, but the molecular and cellular mechanisms underlying this phenomenon have not yet been fully explained. Increasing scientific evidence is stressing the pivotal role of astrocyte dysfunction in the pathogenesis of a wide range of neurological disorders. In light of the above, the aim of this study was to develop an in vitro model of cobalamin deficiency by optimizing the conditions of astrocyte culture in the presence of vitamin B12 antagonist, and then the model was used for multidirectional analysis of astrocyte homeostasis using image cytometry, immunoenzymatic and colorimetric assays, and fluorescence spectroscopy. Our results indicated that long-term incubation of normal human astrocytes with hydroxycobalamin(c-lactam) causes an increase of extracellular homocysteine level, a reduction of cell proliferation, and an accumulation of cells in the G2/M cell cycle phase. Moreover, we observed dramatic activation of caspases and an increase of catalase activity. Interestingly, we excluded extensive apoptosis and oxidative stress. The study provided significant evidence for astrocyte homeostasis disturbance under hypocobalaminemia, thus indicating an important element of the molecular mechanism of nervous system diseases related to vitamin B12 deficiency.

show abstract

Ciprofloxacin-mediated induction of S-phase cell cycle arrest and apoptosis in COLO829 melanoma cells

Abstract: The obtained results for COLO829 melanoma cells were compared with data for normal dark pigmented melanocytes and the use of ciprofloxacin as a potential anticancer drug for the treatment of melanoma in vivo was considered.

Cited by 53 publications

References 32 publications

Ciprofloxacin triggers the apoptosis of human triple-negative breast cancer MDA-MB-231 cells via the p53/Bax/Bcl-2 signaling pathway

Ciprofloxacin triggers the apoptosis of human triple-negative breast cancer MDA-MB-231 cells via the p53/Bax/Bcl-2 signaling pathway

Antibiotics for cancer treatment: A double-edged sword

Cobalamin Deficiency: Effect on Homeostasis of Cultured Human Astrocytes

Contact Info

Product

Resources

About