Society of University SurgeonsNF-κB–mediated chemoresistance in breast cancer cells*,**
Section snippets
Cell culture
The MCF-7 cell variant APO− (previously designated “M,” passage 180) and the MCF-7 APO+ cell variant (previously designated “N,” passage 50) have been previously described13, 14; and these cells were maintained as outlined by Burow et al.13 Cells were plated in 25 cm2 (T-25) and 75 cm2 (T-75) Falcon (BD Biosciences, Bedford, Mass) tissue culture flasks, 6-well plates, 12-well plates, or 96-well plates.
Reagents
The following chemicals were used: TNF (R&D Systems, Minneapolis, Minn), PAC (Biomol, Plymouth
Determination of NF-κB/LUC dose response
Given the role of NF-κB in mediating cell survival despite chemotherapeutic-induced apoptosis, we initially attempted to determine whether differences in basal NF-κB activity exist among the previously described APO− and APO+ MCF-7 cell variants. Basal NF-κB activity was determined in the APO+ and APO− cells by using an NF-κB/LUC reporter assay (Fig 1).
Discussion
It has been implicated that the transcription factor NF-κB is responsible for regulating a host of molecular determinants that have been shown to activate cellular-survival machinery and gene expression.8 The survival cascades initiated by this transcription factor have been shown to be a key component of cellular apoptotic resistance.3, 4, 5, 6, 7 Our previous research efforts have partly concentrated on the identification and characterization of phenotypically different MCF-7 breast
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2013, BiomaterialsCitation Excerpt :The high interference efficiency, together with the lack of cytotoxicity, suggested that TSP had potential for use in RNAi therapies in vivo. Activation of NF-κB has been reported to be associated with resistance to apoptosis [23,24]. To investigate whether blockade of NF-κB signaling pathway by TSNs could induce cell apoptosis, the cellular and nuclear morphology was observed using a fluorescence inversion microscope system.
Hydrogen sulfide-releasing aspirin suppresses NF-κB signaling in estrogen receptor negative breast cancer cells in vitro and in vivo
2012, Biochemical PharmacologyCitation Excerpt :NF-κB binds to DNA and leads to transcription of genes that contribute to tumorigenesis, such as inflammatory, antiapoptotic genes, and positive regulators of cell proliferation and angiogenesis, and in promoting metastasis in vivo [19,20]. Studies indicate that NF-κB is constitutively activated in estrogen receptor-negative breast cancer cell lines and primary tumors [21–24], and that this event is associated with resistance to apoptosis [25,26], and promotion of an invasive and metastatic phenotype [27]. In several mouse xenograft models, tumor growth is impaired when NF-κB is inhibited [20,28,29].
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Supported by National Institutes of Health grant 1-T32-CA65436-01A3 (B. M. J.), U.S. Department of Defense Army Breast Cancer Research fellowship DAMD17-97-1-7024 (M. E. B.), the Cancer Association of Greater New Orleans (M. E. B., B. S. B.), the Tulane Cancer Center (B. S. B.), and the Center for Bioenvironmental Research at Tulane and Xavier Universities (B. S. B., M. E. B.).
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Reprint requests: Bernard M. Jaffe, MD, Department of Surgery, Tulane University School of Medicine, Tulane University Health Sciences Center, 1430 Tulane Ave, SL-22, New Orleans, LA 70112.