Patterns of gene expressions induced by arsenic trioxide in cultured human fibroblasts

Burnichon, Vanina; Jean, Stéphane; Bellon, L.; Maraninchi, Marie; Bideau, Chantal; Orsière, Thierry; Margotat, Alain; Gérolami, V.; Botta, A.; Bergé-Lefranc, Jean-Louis

doi:10.1016/s0378-4274(03)00171-1

Cited by 22 publications

(11 citation statements)

References 28 publications

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“…Recent report indicates that up to 20 mM of As 2 O 3 does not significantly affect cell viability in cultured human fibroblasts [Burnichon et al, 2003], and we also confirmed no effects of 2 mM As 2 O 3 or As 4 O 6 treatment on cell viability of human dermal fibroblast (data not shown). Therefore, it is highly unlikely that arsenical compounds would have nonspecific antimitogenic activity on normal cells.…”

Section: Discussionsupporting

confidence: 87%

Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF‐ and VEGF‐induced proliferation of human endothelial cells

Woo

Park

et al. 2005

J of Cellular Biochemistry

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Arsenic trioxide (As2O3, diarsenic oxide) has recently been reported to induce apoptosis and inhibit the proliferation of various human cancer cells derived from solid tumors as well as hematopoietic malignancies. In this study, the in vitro effects of As2O3 and tetraasrsenic oxide (As4O6) on cell cycle regulation and basic fibroblast growth factor (bFGF)- or vascular endothelial growth factor (VEGF)-stimulated cell proliferation of human umbilical vein endothelial cells (HUVEC) were investigated. Significant dose-dependent inhibition of cell proliferation was observed when HUVEC were treated with either arsenical compound for 48 h, and flow cytometric analysis revealed that these two arsenical compounds induced cell cycle arrest at the G1 and G2/M phases--the increases in cell population at the G1 and G2/M phase were dominantly observed in As2O3- and As4O6-treated cells, respectively. In both arsenical compounds-treated cells, the protein levels of cyclin A and CDC25C were significantly reduced in a dose-dependent manner, concomitant to the reduced activities of CDK2- and CDC2-associated kinase. In G1-synchronized HUVEC, the arsenical compounds prevented the cell cycle progression from G1 to S phase, which was stimulated by bFGF or VEGF, through the inhibition of growth factor-dependent signaling. These results suggest that arsenical compounds inhibit the proliferation of HUVEC via G1 and G2/M phase arrest of the cell cycle. In addition, these inhibitory effects on bFGF- or VEGF-stimulated cell proliferation suggest antiangiogenic potential of these arsenical compounds.

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Section: Discussionsupporting

confidence: 87%

Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF‐ and VEGF‐induced proliferation of human endothelial cells

Woo

Park

et al. 2005

J of Cellular Biochemistry

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“…Some studies showed that As 2 O 3 achieve anti-tumor activity by inhibiting AP-1 [4,23]. However, there are different reports that As 2 O 3 stimulated the activity of the AP-1 in cultured human fibroblasts [24] and acute promyelocytic leukemia [25]. Paradoxical results may be existed in various cells treated by As 2 O 3 because many arsenic properties share in both anti-cancer and pro-cancer.…”

Section: Discussionmentioning

confidence: 99%

Arsenic trioxide inhibits cell proliferation and human papillomavirus oncogene expression in cervical cancer cells

Wang¹,

Gao²,

Zheng³

2014

Biochemical and Biophysical Research Communications

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“…The microarray technology has also been applied by other investigators to analyze genes potentially relevant for cellular response towards arsenic trioxide [46]–[49]. In these studies, the gene expression between untreated and arsenic trioxide-treated cell lines has been compared to identify genes up- or down-regulated upon drug challenge.…”

Section: Discussionmentioning

confidence: 99%

“…These include cell cycle-regulating genes [46−49], transcription factors and cofactors [47], [49], signal transducers [46], [50], DNA repair genes [46], [49] and apoptosis-regulating genes [47]. This indicates that these cellular functions may be of importance for resistance to arsenic trioxide.…”

Section: Discussionmentioning

confidence: 99%

Factors Determining Sensitivity and Resistance of Tumor Cells to Arsenic Trioxide

et al. 2012

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Previously, arsenic trioxide showed impressive regression rates of acute promyelocytic leukemia. Here, we investigated molecular determinants of sensitivity and resistance of cell lines of different tumor types towards arsenic trioxide. Arsenic trioxide was the most cytotoxic compound among 8 arsenicals investigated in the NCI cell line panel. We correlated transcriptome-wide microarray-based mRNA expression to the IC50 values for arsenic trioxide by bioinformatic approaches (COMPARE and hierarchical cluster analyses, Ingenuity signaling pathway analysis). Among the identified pathways were signaling routes for p53, integrin-linked kinase, and actin cytoskeleton. Genes from these pathways significantly predicted cellular response to arsenic trioxide. Then, we analyzed whether classical drug resistance factors may also play a role for arsenic trioxide. Cell lines transfected with cDNAs for catalase, thioredoxin, or the anti-apoptotic bcl-2 gene were more resistant to arsenic trioxide than mock vector transfected cells. Multidrug-resistant cells overexpressing the MDR1, MRP1 or BCRP genes were not cross-resistant to arsenic trioxide. Our approach revealed that response of tumor cells towards arsenic trioxide is multi-factorial.

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Patterns of gene expressions induced by arsenic trioxide in cultured human fibroblasts

Cited by 22 publications

References 28 publications

Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF‐ and VEGF‐induced proliferation of human endothelial cells

Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF‐ and VEGF‐induced proliferation of human endothelial cells

Arsenic trioxide inhibits cell proliferation and human papillomavirus oncogene expression in cervical cancer cells

Factors Determining Sensitivity and Resistance of Tumor Cells to Arsenic Trioxide

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