Arsenic Trioxide-Induced Growth Arrest of Breast Cancer MCF-7 Cells Involving FOXO3a and IκB Kinase β Expression and Localization

Liu, Wenlou; Gong, Yu-Sen; Li, Haili; Jiang, Guan; Zhan, Shining; Liu, Hong; Wu, Yongping

doi:10.1089/cbr.2012.1162

Cited by 16 publications

(15 citation statements)

References 34 publications

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“…Our data do not preclude the possibility that FOXO3 may interact with other NF-κB family members under different conditions. In fact, it was previously shown in a model of inflammation that FOXO3 inhibited NF-κB activity and the mechanism was found to include interaction with IκB (23). Our results demonstrate IκB does not co-precipitate with FOXO3 in TA-DC (Fig.…”

Section: Resultsmentioning

confidence: 99%

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FOXO3–NF-κB RelA Protein Complexes Reduce Proinflammatory Cell Signaling and Function

Thompson

Larson

Vidrine

et al. 2015

The Journal of Immunology

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Tumor-associated myeloid cells, including dendritic cells and macrophages, are immune suppressive. The current study demonstrates a novel mechanism involving FOXO3 and NF-κB RelA that controls myeloid cell signaling and impacts their immune suppressive nature. We find that FOXO3 binds NF-κB RelA in the cytosol, impacting both proteins by preventing FOXO3 degradation and preventing NF-κB RelA nuclear translocation. The location of protein-protein interaction was determined to be near the FOXO3 transactivation domain. In turn, NF-κB RelA activation was restored upon deletion of the same sequence in FOXO3 containing the DNA binding domain. We have identified for the first time, a direct protein-protein interaction between FOXO3 and NF-κB RelA in tumor-associated dendritic cells. These detailed biochemical interactions provide the foundation for future studies to utilize the FOXO3-NF-κB RelA interaction as a target to enhance tumor-associated dendritic cell function to support or enhance anti-tumor immunity.

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Section: Resultsmentioning

confidence: 99%

“…These data confirm a previous report by Lin et.al . demonstrating FOXO3-suppressed NF-κB activation in T cells, where hyper-activation of NF-κB in FOXO3 -/- mice resulted in autoimmune disease (23). …”

Section: Resultsmentioning

confidence: 99%

FOXO3–NF-κB RelA Protein Complexes Reduce Proinflammatory Cell Signaling and Function

Thompson

Larson

Vidrine

et al. 2015

The Journal of Immunology

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“…In addition to APL, the antitumor activity of ATO has been reported in a variety of solid tumor cell lines including breast, esophageal, cervical, lung, liver, prostate and liver carcinoma (8)(9)(10)(11)(12)(13). However, it was reported that many solid tumors are less sensitive to ATO than APL.…”

Section: Discussionmentioning

confidence: 99%

“…It is now well established that ATO induces complete remission in 80-90% of newly diagnosed patients with APL, as well as in 60-90% of all-trans retinoic acid refractory patients (5)(6)(7). Furthermore, the anticancer activity of ATO was also intensively studied in various other hematological malignancies and several solid tumors, including breast cancer (8)(9)(10)(11)(12)(13). Although ATO is very effective in the treatment of APL, ATO has been less successful in other malignancies at tolerable doses.…”

Section: Introductionmentioning

confidence: 99%

Cotylenin A and arsenic trioxide cooperatively suppress cell proliferation and cell invasion activity in human breast cancer cells

Kasukabe

Okabe‐Kado

Kato

et al. 2014

International Journal of Oncology

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Abstract. Arsenic trioxide (ATO) is an approved treatment for acute promyelocytic leukemia (APL). It has also shown potential for treatment of multiple myeloma and various solid tumors including breast cancer. The requirement of high, toxic concentrations for the induction of apoptosis in non-APL and solid tumor cells is a major limitation for its use in other hematological malignancies and solid tumors. We have examined whether inducers of differentiation of leukemia cells can control the growth of solid tumor cells. In the present study, we found that cotylenin A, a plant growth regulator and a potent inducer of differentiation in myeloid leukemia cells, significantly potentiated both ATO-induced inhibition of cell growth in a liquid culture, and ATO-induced inhibition of anchorageindependent growth in a semi-solid culture in human breast cancer MCF-7 and MDA-MB-231 cells. ISIR-005 (a synthetic cotylenin A-derivative) was also able to enhance ATO-induced growth inhibition. The combined treatment with cotylenin A and ATO induced cleaved caspase-7 in MCF-7 cells at the concentrations which ATO alone scarcely induced and cotylenin A alone only weakly induced. Expression of survivin in MCF-7 cells was markedly decreased with the presence of both cotylenin A and ATO, although the expression of survivin was only slightly decreased by cotylenin A or ATO alone. The pretreatment with N-acetylcysteine significantly reduced the combination treatment-induced cell growth inhibition. These data suggest that induction of cleaved caspase-7, inhibition of survivin and oxidative responses are important events in the corporative inhibition in the growth of MCF-7 cells induced by both cotylenin A and ATO. Furthermore, we found that the combined treatment with cotylenin A and ATO also could be effective in suppressing the invasive capacity of MDA-MB-231 cells determined with the impedance-based xCELLigence Real-Time Cell Analysis technology. These results suggest that cotylenin A is an attractive enhancer for the ATO-induced anticancer activities in human breast cancer.

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“…10 ATO induced cell growth arrest via regulation of FOXO3a (forkhead box O3a) and IKKb (Ikb kinase b) expression and localization in breast cancer cells. 11 ATO induced cell apoptosis via activation of caspase-3 and suppression of HERG (human ether-a-go-go-related gene) channels in breast cancer cells. 12 These reports indicated that ATO exerts its functions via regulation of cell signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide inhibits cell growth and motility via up-regulation of let-7a in breast cancer cells

et al. 2017

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Arsenic trioxide (ATO) has been reported to exert its anti-cancer activities in human cancers. However, the molecular mechanism of ATO-triggered anti-tumor activity has not been fully elucidated. Recently, multiple studies demonstrated that ATO could regulate miRNAs in human cancers. Therefore, in this study, we investigated whether ATO regulated let-7a in breast cancer cells. We found that ATO upregulated let-7a level in breast cancer cells. We also found that up-regulation of let-7a inhibited cell growth and induced apoptosis and retarded cell migration and invasion. We also observed that up-regulation of let-7a enhanced cell growth inhibition and invasion suppression induced by ATO treatment. Our findings suggest that ATO suppressed cell growth, stimulated apoptosis, and retarded cell invasion partly via upregulation of let-7a in breast cancer cells. Our study provides a new anti-tumor mechanism of ATO treatment in breast cancer.

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Arsenic Trioxide-Induced Growth Arrest of Breast Cancer MCF-7 Cells Involving FOXO3a and IκB Kinase β Expression and Localization

Cited by 16 publications

References 34 publications

FOXO3–NF-κB RelA Protein Complexes Reduce Proinflammatory Cell Signaling and Function

FOXO3–NF-κB RelA Protein Complexes Reduce Proinflammatory Cell Signaling and Function

Cotylenin A and arsenic trioxide cooperatively suppress cell proliferation and cell invasion activity in human breast cancer cells

Arsenic trioxide inhibits cell growth and motility via up-regulation of let-7a in breast cancer cells

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