NF-κB Directly Regulates Fas Transcription to Modulate Fas-mediated Apoptosis and Tumor Suppression

Liu, Feiyan; Bardhan, Kankana; Yang, Dafeng; Thangaraju, Muthusamy; Ganapathy, Vadivel; Waller, Jennifer L.; Liles, Georgia; Lee, Jeffrey R.; Liu, Kebin

doi:10.1074/jbc.m112.356279

Cited by 140 publications

(119 citation statements)

References 60 publications

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“…p65/RelA binds to the FAS gene promoter, whereas NF-kB inhibition with either BAY11-7082 (33) hepatocytes (6,20), and various solid tumor cell types (11,32). The cell context may be essential as NF-kB activation through the alternate pathway could be a FAS transcription repressor in murine erythroleukemia (MEL) cells (34). Alternatively, the threshold of NF-kB activity, which is under control of either the quantity of dimers p65/ p65, p50/p50, and p65/p50 recruited to the chromatin or posttranslational modifications, or interactions with other transcription factors such as Sp1 could determine its effects (35,36).…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Ettou

Humbrecht

Benet

et al. 2013

Molecular Cancer Research

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The death domain containing TNF receptor 6 (CD95/Fas) is a direct target for the NF-kB transcription factor and is repressed in solid tumors such as colon carcinomas. Previously, we reported that the Fas death receptor, while overexpressed in low-risk myelodysplastic syndromes (MDS), becomes undetectable on CD34 þ progenitors when the disease progresses to secondary acute myeloid leukemia (AML). This study determined the interplay between NF-kB and Fas during MDS progression. We first observed that Fas was induced by TNF-a in the HL60 cell line. In these cells, p65 (RELA) was associated with the FAS promoter, and inhibition of the NF-kB pathway by an IKKa inhibitor (BAY11-7082) or lentiviral expression of a nondegradable mutant of IkBa (IkSR)

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Section: Discussionmentioning

confidence: 99%

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Ettou

Humbrecht

Benet

et al. 2013

Molecular Cancer Research

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“…V-ATPase On the one hand, lactate supports tumor growth, cell migration, and metastasis [147][148][149][150] . One of the suggested mechanism is its interaction with NF-kappaB 151,152 . On the other hand, lactate is associated with spontaneous regression of cancer when exogenously administrated 153 .…”

Section: Vacuolar Atpase (V-atpase)mentioning

confidence: 99%

Tumor metabolism, cancer cell transporters, and microenvironmental resistance

Alfarouk

2016

Journal of Enzyme Inhibition and Medicinal Chemistry

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Cancer cells reprogram their metabolic machineries to enter into permanent glycolytic pathways. The full reason for such reprogramming takes place is unclear. However, this metabolic switch is not made in vain for the lactate that is generated and exported outside cells is reused by other cells. This results in the generation of a pH gradient between the low extracellular pH that is acidic (pHe) and the higher cytosolic alkaline or near neutral pH (pHi) environments that are tightly regulated by the overexpression of several pumps and ion channels (e.g. NHE-1, MCT-1, V-ATPase, CA9, and CA12). The generation of this unique pH gradient serves as a determining factor in defining ''tumor fitness''. Tumor fitness is the capacity of the tumor to invade and metastasize due to its ability to reduce the efficiency of the immune system and confer resistance to chemotherapy. In this article, we highlight the importance of tumor microenvironment in mediating the failure of chemotherapeutic agents.

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“…41 A previous study illustrated that in addition to inflammation, NFkB can also be associated with cancer progression, including cell apoptosis, cell cycle regulation, differentiation, and migration. 42 Nevertheless, the role of 43 Additionally, it has been well established that NFkB can affect colon cancer progression through the regulation of many associated genes such as cyclin D1, Bcl-XL, VEGF, IL-8, COX-2, and MMP-9. 44 Most importantly, the current drugs used for colon cancer therapy have been demonstrated to be able to regulate NFkB expression which, in turn, inhibit cancer cell proliferation and migration.…”

Section: Mechanism Of Signal Transduction Initiationmentioning

confidence: 99%

Inhibition of colon cancer cell growth by nanoemulsion carrying gold nanoparticles and lycopene

Huang¹,

Wei²,

Inbaraj³

et al. 2015

IJN

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Lycopene (LP), an important functional compound in tomatoes, and gold nanoparticles (AN), have received considerable attention as potential candidates for cancer therapy. However, the extreme instability and poor bioavailability of LP limits its in vivo application. This study intends to develop a nanoemulsion system incorporating both LP and AN, and to study the possible synergistic effects on the inhibition of the HT-29 colon cancer cell line. LP–nanogold nanoemulsion containing Tween 80 as an emulsifier was prepared, followed by characterization using transmission electron microscopy (TEM), dynamic light scattering (DLS) analysis, ultraviolet spectroscopy, and zeta potential analysis. The particle size as determined by TEM and DLS was 21.3±3.7 nm and 25.0±4.2 nm for nanoemulsion and 4.7±1.1 nm and 3.3±0.6 nm for AN, while the zeta potential of nanoemulsion and AN was −32.2±1.8 mV and −48.5±2.7 mV, respectively. Compared with the control treatment, both the combo (AN 10 ppm plus LP 12 μM) and nanoemulsion (AN 0.16 ppm plus LP 0.4 μM) treatments resulted in a five- and 15-fold rise in early apoptotic cells of HT-29, respectively. Also, the nanoemulsion significantly reduced the expressions of procaspases 8, 3, and 9, as well as PARP-1 and Bcl-2, while Bax expression was enhanced. A fivefold decline in the migration capability of HT-29 cells was observed for this nanoemulsion when compared to control, with the invasion-associated markers being significantly reversed through the upregulation of the epithelial marker E-cadherin and downregulation of Akt, nuclear factor kappa B, pro-matrix metalloproteinase (MMP)-2, and active MMP-9 expressions. The TEM images revealed that numerous nanoemulsion-filled vacuoles invaded cytosol and converged into the mitochondria, resulting in an abnormally elongated morphology with reduced cristae and matrix contents, demonstrating a possible passive targeting effect. The nanoemulsion containing vacuoles were engulfed and internalized by the nuclear membrane envelop for subsequent invasion into the nucleoli. Taken together, LP–nanogold nanoemulsion could provide synergistic effects at AN and LP doses 250 and 120 times lower than that in the combo treatment, respectively, demonstrating the potential of nanoemulsion developed in this study for a possible application in colon cancer therapy.

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NF-κB Directly Regulates Fas Transcription to Modulate Fas-mediated Apoptosis and Tumor Suppression

Cited by 140 publications

References 60 publications

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Tumor metabolism, cancer cell transporters, and microenvironmental resistance

Inhibition of colon cancer cell growth by nanoemulsion carrying gold nanoparticles and lycopene

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NF-κB Directly Regulates Fas Transcription to Modulate Fas-mediated Apoptosis and Tumor Suppression

Cited by 140 publications

References 60 publications

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Epigenetic Control of NF-κB-Dependent FAS Gene Transcription during Progression of Myelodysplastic Syndromes

Tumor metabolism, cancer cell transporters, and microenvironmental resistance

Inhibition of colon cancer cell growth by nanoemulsion carrying gold nanoparticles and&nbsp;lycopene

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Inhibition of colon cancer cell growth by nanoemulsion carrying gold nanoparticles and lycopene