Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-κB

Riley, P. A.; Frisch, Steven M.

doi:10.1007/s10495-013-0847-1

Cited by 44 publications

(48 citation statements)

References 49 publications

(60 reference statements)

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“…We next examined the nuclear translocation of NF-κB p65, and NF-κB luciferase reporter activity ( Figure 9A). In addition, the protein levels of NF-κB target genes, such as matrix metallopeptidase 9 (MMP9) and cellular FLICE-inhibitory protein (c-FLIP), which are involved in cancer cell invasion and anoikis resistance (29)(30)(31), were increased following IRX1 overexpression. In contrast, IRX1 knockdown in ZOSM and 143B cells significantly decreased NF-κB p65 nuclear translocation, NF-κB-luciferase reporter activity, and expression of MMP9 and c-FLIP ( Figure 9A).…”

Section: Nf-κb Pathway Activation Is Involved In Irx1/cxcl14-induced mentioning

confidence: 99%

IRX1 hypomethylation promotes osteosarcoma metastasis via induction of CXCL14/NF-κB signaling

Lu¹,

Song²,

Tang³

et al. 2015

J. Clin. Invest.

111

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Section: Nf-κb Pathway Activation Is Involved In Irx1/cxcl14-induced mentioning

confidence: 99%

IRX1 hypomethylation promotes osteosarcoma metastasis via induction of CXCL14/NF-κB signaling

Lu¹,

Song²,

Tang³

et al. 2015

J. Clin. Invest.

111

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“…To acquire a metastatic potential, CTCs must develop resistance to anoikis [11–13]. The adaptive processes that help CTCs evade anoikis include EMT [14,15], metabolic changes and antioxidant activity [16–18], activation of receptor tyrosine kinases [19–22], activation of the NF-κB pathway [23,24], activation of YAP/TAZ transcription coactivators [25,26], or increased autophagy [27–30]. …”

Section: Introductionmentioning

confidence: 99%

Protein disulfide isomerases in the endoplasmic reticulum promote anchorage-independent growth of breast cancer cells

Wise

Duhachek-Muggy

et al. 2016

Breast Cancer Res Treat

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Purpose Metastatic breast cancer cells are exposed to stress of detachment from the extracellular matrix (ECM). Cultured breast cancer cells that survive this stress and are capable of anchorage-independent proliferation form mammospheres. The purpose of this study was to explore a link between mammosphere growth, ECM gene expression, and the protein quality control system in the endoplasmic reticulum (ER). Methods We compared the mRNA and protein levels of ER folding factors in SUM159PT and MCF10DCIS.com breast cancer cells grown as mammospheres versus adherent conditions. Publicly available gene expression data for mammospheres formed by primary breast cancer cells and for circulating tumor cells (CTCs) were analyzed to assess the status of ECM/ER folding factor genes in clinically relevant samples. Knock-down of selected protein disulfide isomerase (PDI) family members was performed to examine their roles in SUM159PT mammosphere growth. Results Cells grown as mammospheres had elevated expression of ECM genes and ER folding quality control genes. CTC gene expression data for an index patient indicated that upregulation of ECM and ER folding factor genes occurred at the time of acquired therapy resistance and disease progression. Knock-down of PDI, ERp44, or ERp57, three members of the PDI family with elevated protein levels in mammospheres, in SUM159PT cells partially inhibited the mammosphere growth. Conclusion Breast cancer cell survival and growth under detachment conditions require enhanced assistance of the ER protein folding machinery. Targeting ER folding factors, in particular members of the PDI family, may improve the therapeutic outcomes in metastatic breast cancer.

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“…DBC1 directly interacted with the catalytic domain of SIRT1, thereby inhibiting SIRT1 activities [24]. Moreover, DBC1 is thought to be one key co-factor for the mediation of the IKK-β-NF-κB signaling pathway [25]. DBC1/SIRT1 complex may act an important role in regulation of aging and inflammatory responses.…”

Section: Resultsmentioning

confidence: 99%

“…It has been well documented that one of the SIRT1 downstream gene, DBC1, is a main negative regulator of SIRT1 [24]. In addition, DBC1 is associated with IKK-β to increase NF-κB transcriptional activities [25]. Calliari et al reported SIRT1 activation mitigates neurodegeneration through DBC1inhibition [48].…”

Section: Discussionmentioning

confidence: 99%

The potential role of epigenetic modulations in BPPV maneuver exercises

et al. 2016

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Benign paroxysmal positional vertigo (BPPV) is one of the most common complaints encountered in clinics and is strongly correlated with advanced age or, possibly, degeneration. Redistribution exercises are the most effective approaches to treat BPPV, and canalith repositioning procedure (CRP) cure most BPPV cases. However, the mechanisms through which the treatment modulates systemic molecules in BPPV patients remain largely unknown. In this study, we report that the miR-34a and Sirtuin 1 (SIRT1) genes correlated with the treatment effects of CRP in BPPV subjects. We found that miR-34a expression was largely inhibited and SIRT1 expression was significantly reversed after BPPV maneuver treatment. We also confirmed that the PPAR-γ, PGC-1 and FoxO gene expressions were decreased immediately after canalith repositioning procedure (CRP) for BPPV, and were largely increased after a complete cure of BPPV. Moreover, we observed that after a complete recovery of BPPV, the ROS concentrations, pro-inflammatory cytokine concentrations and p53 expression levels were attenuated. We conclude that BPPV treatment might involve some epigenetic regulations through the mediation of miR-34a, SIRT1 functions and repression of redox status.

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Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-κB

Cited by 44 publications

References 49 publications

IRX1 hypomethylation promotes osteosarcoma metastasis via induction of CXCL14/NF-κB signaling

IRX1 hypomethylation promotes osteosarcoma metastasis via induction of CXCL14/NF-κB signaling

Protein disulfide isomerases in the endoplasmic reticulum promote anchorage-independent growth of breast cancer cells

The potential role of epigenetic modulations in BPPV maneuver exercises

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