Effect of arsenic trioxide (Trisenox) on actin organization in K-562 erythroleukemia cells.

Izdebska, Magdalena; Grzanka, Alina; Ostrowski, Maciej; Żuryń, Agnieszka; Grzanka, Dariusz

doi:10.2478/v10042-009-0080-5

Cited by 6 publications

(5 citation statements)

References 41 publications

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“…It is known, that actin and actin-binding proteins are involved in chromatin remodeling and gene transcription. In our previous study, we observed that actin was associated with the heterochromatin during apoptosis (38,46,47). Moreover, Zhao et al showed that F-actin is directly involved in the chromatin reorganization (48).…”

Section: Discussionmentioning

confidence: 94%

The effect of G-CSF on F-actin reorganization in HL-60 and K562 cell lines

et al. 2012

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The aim of this investigation was to show the influence of G-CSF (G-CSF) on the F-actin cytoskeleton and the morphology of G-CSFR-proficient HL-60 and G-CSFR-deficient K562 cell lines. In the present study, we show changes in F-actin distribution in HL-60 cells after treatment with 5 and 10 ng/ml concentration of G-CSF but also changes in the organization and fluorescence intensity of F-actin in the K562 cell line. After treatment of HL-60 cells with 5 ng/ml concentration of G-CSF we observed an increase in F-actin levels. Additionally, a higher labeling of nuclear F-actin under TEM was observed. Moreover, changes in the cell cycle indicate cell differentiation. On the other hand, in the K562 cell line we observed an increase in the percentage sub-G1 cells following treatment with both concentration of G-CSF. Furthermore, an increase in the percentage of late apoptotic cells after G-CSF treatment was observed. A statistically significant difference in the cytoplasmic F-actin levels was not detected, but nuclear levels were decreased. In conclusion, we suggest that the G-CSF-based reorganization of actin filaments in HL-60 cells is involved in the differentiation process. Moreover, we suggest that the G-CSF-induced changes observed in K562 cells are associated with a G-CSF receptor-independent pathway or its binding to other similar receptors.

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Section: Discussionmentioning

confidence: 94%

The effect of G-CSF on F-actin reorganization in HL-60 and K562 cell lines

et al. 2012

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“…Because As 2 O 3 at higher concentrations induces many side effects and chronic arsenic exposure is linked to carcinogenesis, low-dose combination therapy is required (27,28). Together with increasing doses, As 2 O 3 caused an increase in the number of cells undergoing apoptosis (29). In our study, a low-dose combination of two chemotherapeutic agents (300 µg/mL TMP plus 0.5 µM As 2 O 3 ) markedly decreased cell viability and induced differentiation throughout the cell cycle, as detected by a slower rate of accumulation in G0/G1.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine potentiates arsenic trioxide activity against HL-60 cell lines

You-hua

Shen

et al. 2012

Braz J Med Biol Res

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“…reactive oxygen species (ROS) and reactive nitrogen species (RNS)] and molecular parameters of biological response (e.g. plasma membrane composition, actin microfilaments and activated diphosphorilated c‐Jun N‐terminal kinase (JNK)] and cellular viability are essential [10].…”

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confidence: 99%

Modulation of Early Stress‐related Biomarkers in Cytoplasm by the Antioxidants Silymarin and Quercetin Using a Cellular Model of Acute Arsenic Poisoning

Soria

Eynard

Bongiovanni

2010

Basic Clin Pharma Tox

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Several pathologies (e.g. cancer and diabetes) are increased in arsenic-exposed populations, with oxidative stress being a major toxicological mechanism. Since the flavonoids silymarin (S) and quercetin (Q) are antioxidants and may protect cells, it would be valuable to develop a model which allows assessing the potential of xenobiotic against arsenic cytotoxicity in an efficient and rapid way. Thus, the oxidant production [e.g. reactive oxygen species and reactive nitrogen species (RNS)], the molecular parameters of biological response [e.g. plasma membrane composition, actin microfilaments and activated diphosphorilated c-Jun N-terminal kinase (JNK)] and cellular viability were determined in CHO-K1 cells treated with arsenite (As), S and Q. Arsenic caused loss of the cellular viability in a time-dependent manner. This effect was accompanied by a lipid hydroperoxide (LHP) formation, with no RNS induction or ganglioside content changes being found. Both flavonoids counteracted oxidative damage. Despite all treatments had unspecific responses on nitrite cellular release along the time, there was no relation between them and the cellular viability. Arsenic induced cytoplasmic microfilament rearrangement (tight perinuclear distribution with projections, stress fibres and pseudopodia) which was reversed by S. Also, activated JNK showed a similar distribution to actin. Contrarily, Q caused a dysmorphic granular pattern, thus behaving as a toxic agent. Summing up, toxic levels of arsenic disturb the redox homeostasis with LHP induction and early triggering of stress responses in cytoskeleton and cell signalling. Using the proposed model, only S showed to protect cells from arsenical cytotoxicity without own toxic properties. Thus, S might be considered for modulation of the human arsenic susceptibility.

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Effect of arsenic trioxide (Trisenox) on actin organization in K-562 erythroleukemia cells.

Cited by 6 publications

References 41 publications

The effect of G-CSF on F-actin reorganization in HL-60 and K562 cell lines

The effect of G-CSF on F-actin reorganization in HL-60 and K562 cell lines

Tetramethylpyrazine potentiates arsenic trioxide activity against HL-60 cell lines

Modulation of Early Stress‐related Biomarkers in Cytoplasm by the Antioxidants Silymarin and Quercetin Using a Cellular Model of Acute Arsenic Poisoning

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