The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins
Abstract
It has been shown recently in China that arsenic trioxide (As2O3) is a very effective treatment for acute promyelocytic leukemia (APL). APL patients resistant to all-trans retinoic acid (ATRA) and conventional chemotherapy can still respond to AS2O3. In this study, we addressed the possible cellular and molecular mechanisms of this treatment by using NB4 cells as a model. The results show that: (1) As2O3 triggers relatively specific NB4 cell apoptosis at micromolar concentration, as proved by morphology, histogramic related nuclear DNA contents, and DNA gel eletrophoresis. (2) As2O3 does not influence bax, bcl-x, c-myc, and p53 gene expression, but downregulates bcl-2 gene expression at both mRNA and protein levels. (3) As2O3 induces a significant modulation of the PML staining pattern in NB4 cells and HL-60 cells. The micropunctates characteristic of PML-RAR alpha in NB4 cells dissappear after treatment with As2O3, whereas a diffuse PML staining occurs in the perinuclear cytoplasmic region. In addition, a low percentage of untreated NB4 cells exhibits an accumulation of PML positive particles in a compartment of cytoplasm. The percentage of these cells can be significantly increased after As2O3 treatment. A similar PML staining pattern is observed in apoptotic cells. (4) ATRA pretreatment does not influence As2O3-induced apoptosis. These results suggest that induction of cell apoptosis can be one of the mechanisms of the therapeutic effect of As2O3. Moreover, this apoptosis induction occurs independently of the retinoid pathway and may be mediated, at least partly, through the modulation of bcl-2, as well as PML-RAR alpha and/ or PML proteins.
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Citations
Cites
Apoptosis in the Pathogenesis and Treatment of Disease
Thompson, C. B. (1995) · Science · doi:10.1126/science.7878464 · Cited by 6,524
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
Oltval, Z. N., Milliman, C. L., & Korsmeyer, S. J. (1993) · Cell · doi:10.1016/0092-8674(93)90509-o · Cited by 6,003
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
p53-Dependent apoptosis suppresses tumor growth and progression in vivo
Symonds, H., Krall, L., Remington, L., Saenz-Robles, M., Lowe, S., Jacks, T., & Van Dyke, T. (1994) · Cell · doi:10.1016/0092-8674(94)90534-7 · Cited by 880
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Chronic inflammation and oxidative stress in human carcinogenesis
Federico, A., Morgillo, F., Tuccillo, C., Ciardiello, F., & Loguercio, C. (2007) · International Journal of Cancer · doi:10.1002/ijc.23192 · Cited by 1,001
Sanz, M. A., Fenaux, P., Tallman, M. S., Estey, E. H., Löwenberg, B., Naoe, T., Lengfelder, E., Döhner, H., Burnett, A. K., Chen, S.-J., et al. (2019) · Blood · doi:10.1182/blood-2019-01-894980 · Cited by 664
Self-citationTargeting thioredoxin reductase is a basis for cancer therapy by arsenic trioxide
Lu, J., Chew, E.-H., & Holmgren, A. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0701549104 · Cited by 526
Inhibition of Mitochondrial Respiration
Pelicano, H., Feng, L., Zhou, Y., Carew, J. S., Hileman, E. O., Plunkett, W., Keating, M. J., & Huang, P. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m301546200 · Cited by 495
Lazo, G., Kantarjian, H., Estey, E., Thomas, D., O'Brien, S., & Cortes, J. (2003) · Cancer · doi:10.1002/cncr.11314 · Cited by 494
Metadata
- Authors
- Chen, G., Zhu, J., Shi, X., Ni, J., Zhong, H., Si, G., Jin, X., Tang, W., Li, X., Xong, S., Shen, Z., Sun, G., Ma, J., Zhang, P., Zhang, T., Gazin, C., Naoe, T., Chen, S., Wang, Z., & Chen, Z.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 1996-08-01
- Volume
- 88
- Issue
- 3
- Pages
- 1052-1061
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2184391500
- Cited by
- 864
- References
- 5
- FWCI
- 9.03
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins. https://app.cochat.ai/papers/10.1182/blood.v88.3.1052.1052
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- Chen, G., Zhu, J., Shi, X., Ni, J., Zhong, H., Si, G., Jin, X., Tang, W., Li, X., Xong, S., Shen, Z., Sun, G., Ma, J., Zhang, P., Zhang, T., Gazin, C., Naoe, T., Chen, S., Wang, Z., & Chen, Z. (1996). In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins. Blood. https://doi.org/10.1182/blood.v88.3.1052.1052
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