Induction of p53 protein expression by sodium arsenite

Salazar, Ana María; Ostrosky‐Wegman, Patricia; Menéndez, Daniel; Miranda, Enrique; García‐Carrancá, Alejandro; Rojas, Emilio

doi:10.1016/s0027-5107(97)00207-8

Cited by 80 publications

(32 citation statements)

References 32 publications

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“…stabilization) of p53, as well as its increased degradation, for example by human papillomavirus encoded E6 protein (46), may have oncogenic consequences. Arsenite causes increased abundance of p53 protein (47), a finding consistent with its inhibition of proteosome-dependent proteolysis. Abnormalities in p53 function will cause abnormal control of cell cycle progression, apoptosis and DNA repair (48)(49)(50).…”

Section: Expression Of Asr1 In Chinese Hamster Cellssupporting

confidence: 57%

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis

Rossman

Wang

1999

Carcinogenesis

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Arsenic is a human carcinogen whose mechanism of action is unknown. Previously, this laboratory demonstrated that arsenite acts as a comutagen by interfering with DNA repair, although a specific DNA repair enzyme sensitive to arsenite has not been identified. A number of stable arsenite-sensitive and arsenite-resistant sublines of Chinese hamster V79 cells have now been isolated. In order to gain understanding of possible targets for arsenite's action, one arsenite-resistant subline, As/R28A, was chosen as a donor for a cDNA expression library. The library from arsenite-induced As/R28A cells was transfected into arsenite-sensitive As/S5 cells, and transfectants were selected for arsenite-resistance. Two cDNAs, asr1 and asr2, which confer arsenite resistance to arsenite-hypersensitive As/S5 cells as well as to wild-type cells, were isolated. asr1 shows almost complete homology with the rat fau gene, a tumor suppressor gene which contains a ubiquitin-like region fused to S30 ribosomal protein. Arsenite was previously shown to inhibit ubiquitin-dependent proteolysis. These results suggest that the tumor suppressor fau gene product or some other aspect of the ubiquitin system may be a target for arsenic toxicity and that disruption of the ubiquitin system may contribute to the genotoxicity and carcinogenicity of arsenite.

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Section: Expression Of Asr1 In Chinese Hamster Cellssupporting

confidence: 57%

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis

Rossman

Wang

1999

Carcinogenesis

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“…Further support was reported in studies of arsenic trioxideinduced apoptosis in myeloma cells [37]. Our results are in agreement with a study reporting that exposure of HeLa cells to increasing concentrations (0.1-100 μM) of arsenite for 24 h resulted in a dose-dependent increase in the level of p53 protein expression [38] and were also in agreement with a study reporting that human B lymphoma cell proliferation was inhibited by upregulating p53 expression to induce cell apoptosis [39]. By contrast, Hamadeh et al [40] observed that exposure to low levels of arsenite (0.01- [41].…”

Section: Discussionsupporting

confidence: 93%

Arsenite-Induced Apoptosis Is Prevented by Selenite in A375 Cell Line

Wang

Guo

2010

Biol Trace Elem Res

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Arsenic trioxide induces apoptosis and clinical remission in patients diagnosed with acute promyelocytic leukemia. The human malignant melanoma A375 cells were treated with NaAsO2 (0.1–130 μM) and also treated with combined 10 μM NaAsO2 and 10 μM Na2SeO3. NaAsO2 arrested cell growth in the G1 phase and induced apoptosis in a concentration- and time-dependent manner. In contrast, administration of Na2SeO3 antagonized the cell growth inhibition and apoptosis induced by NaAsO2. The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3. Thus, our results indicate upregulation of p53 and Bcl-2 play acrucial role in the NaAsO2-induced G1 arrest and apoptosis of A375 cells and that downregulation p53 appears to contribute to the inhibition by Na2SeO3 of the effects induced by NaAsO2.

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“…Results of previous studies indicated that iAs does not act through classic genotoxic and mutagenic mechanisms, but rather may be a tumor promoter that modifies signal transduction pathways involved in cell growth and proliferation (29). iAs III has been shown to modulate expression and/or DNAbinding activities of several key transcription factors, including nuclear factor kappa B (30), tumor suppressor 53 (p53) (31), and activating protein-1 (AP-1) (32)(33)(34). Mechanisms of AP-1 activation by iAs III include stimulation of the mitogen-activated protein kinase (MAPK) cascade with a consequent increase in the expression and/or phosphorylation of the two major AP-1 constituents, c-Jun and cFos (29).…”

Section: Effects Of Methylated Trivalent Arsenicals On Gene Transcripmentioning

confidence: 99%

The Role of Biomethylation in Toxicity and Carcinogenicity of Arsenic: A Research Update

Stýblo¹,

Drobná²,

Jaspers³

et al. 2002

Environ Health Perspect

233

132

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Induction of p53 protein expression by sodium arsenite

Cited by 80 publications

References 32 publications

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis

Arsenite-Induced Apoptosis Is Prevented by Selenite in A375 Cell Line

The Role of Biomethylation in Toxicity and Carcinogenicity of Arsenic: A Research Update

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