Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of <i>Twist1</i>

Liu, Yuan; Mayo, Marty W.; Xiao, Aizhen; Hall, Emily H.; Amin, Elianna B.; Kadota, Kyuichi; Adusumilli, Prasad S.; Jones, David R.

doi:10.1128/mcb.00869-14

Cited by 32 publications

(34 citation statements)

References 54 publications

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“…To further validate whether the activation of NF‐κB is dependent on the increased expression of PIK3R1 in DCLK1‐induced EMT, we observed that the downregulation of PIK3R1 blocked the expression levels of p‐Akt, p‐IκB and p‐p65 in DCLK1‐induced cells. Being the important transcription factors and the major regulators in the EMT, ZEB1 and TWIST1 are directly regulated by NF‐κB . The expression levels of ZEB1 and TWIST1, as well as their downstream EMT markers E‐cadherin and Vimentin, were also regulated by PIK3R1 in DCLK1‐induced EMT.…”

Section: Discussionmentioning

confidence: 99%

“…Being the important transcription factors and the major regulators in the EMT, ZEB1 and TWIST1 are directly regulated by NF-jB. 40,41 The expression levels of ZEB1 and TWIST1, as well as their downstream EMT markers E-cadherin and Vimentin, were also regulated by PIK3R1 in DCLK1-induced EMT. Moreover, it has been reported that NF-jB can directly bind the promoter of Vimentin to directly regulate its expression.…”

Section: Discussionmentioning

confidence: 99%

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Retracted: DCLK1 promotes epithelial‐mesenchymal transition via the PI3K/Akt/NF‐κB pathway in colorectal cancer

Liu

Wang

Sun

et al. 2018

Intl Journal of Cancer

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Double cortin-like kinase 1 (DCLK1) plays important roles during the epithelial-mesenchymal transition (EMT) process in human colorectal cancer (CRC). However, the role of DCLK1 in regulating the EMT of CRC is still poorly understood. In this study, we report evidence that DCLK1 acts as a potent oncogene to drive its extremely malignant character of EMT in an NF-κB-dependent manner in CRC cells. Mechanistic investigations showed that DCLK1 induced the NF-κBp65 subunit expression through the PI3K/Akt/Sp1 axis and activated NF-κBp65 through the PI3K/Akt/IκBα pathway during the EMT of CRC cells. Moreover, we found that silencing the expression of DCLK1 inhibited the invasion and metastasis of CRC cells in vivo. Collectively, our findings identify DCLK1 as a pivotal regulator of an EMT axis in CRC, thus implicating DCLK1 as a potential therapeutic target for CRC metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Retracted: DCLK1 promotes epithelial‐mesenchymal transition via the PI3K/Akt/NF‐κB pathway in colorectal cancer

Liu

Wang

Sun

et al. 2018

Intl Journal of Cancer

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“…Human LUAD specimens were obtained with written, informed consent and approval of the Human Investigations Committee at MSKCC. Immunohistochemical analysis was performed as described previously (55). The ADAR antibody was used at a dilution of 1:200.…”

Section: Methodsmentioning

confidence: 99%

The RNA-editing enzyme ADAR promotes lung adenocarcinoma migration and invasion by stabilizing FAK

et al. 2017

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RNA-binding proteins are altered in large-scale, genome-wide cancer studies, although it is unclear how these proteins control tumor progression. Using unbiased gene expression and immunohistochemical analysis of 802 stage I lung adenocarcinoma (LUAD) patients, we show that increased adenosine deaminase acting on double-stranded RNA (ADAR) expression correlates with tumor recurrence. Knockdown of ADAR in LUAD cells reduces mesenchymal properties, cellular migration, and invasion. Analysis of gene expression patterns following the loss of ADAR identifies enrichment in cell migration pathways, most notably focal adhesion kinase (FAK). We show that ADAR posttranscriptionally increases the FAK oncogene through physical interaction with its RNA binding domain and editing a specific intronic site, resulting in stabilization and increase of FAK transcript. Moreover, pharmacological inhibition of FAK blocks ADAR-induced increase of cell invasion in LUAD cells, suggesting a potential therapeutic application for ADAR high-expressing LUAD. Collectively, we identify ADAR as an important regulator of LUAD progression through its ability to stabilize FAK.

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“…The function of EMT in enhancing migration and invasion of cancers has drawn great attention from scientists. During the regulation of EMT, many oncogene and tumor suppressor genes play crucial roles …”

mentioning

confidence: 99%

“…During the regulation of EMT, many oncogene and tumor suppressor genes play crucial roles. (9)(10)(11)(12) The new tumor suppressor gene p53 binding protein 1 (53BP1) has been the research focus of our team over recent years. It is mainly reported as an important regulator of the cellular response to DNA double-strand breaks.…”

mentioning

confidence: 99%

53BP1 suppresses epithelial–mesenchymal transition by downregulating ZEB1 through microRNA‐200b/429 in breast cancer

Kong

Ding

et al. 2015

Cancer Science

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Epithelial–mesenchymal transition (EMT) is an important mechanism of cancer invasion and metastasis. Although p53 binding protein 1 (53BP1) has been implicated in several biological processes, its function in EMT of human cancers has not yet been reported. Here, we show that 53BP1 negatively regulated EMT by modulating ZEB1 through targeting microRNA (miR)-200b and miR-429. Furthermore, 53BP1 promoted ZEB1-mediated upregulation of E-cadherin and also inhibited the expressions of mesenchymal markers, leading to increased migration and invasion in MDA-MB-231 breast cancer cells. Consistently, in MCF-7 breast cancer cells, low 53BP1 expression reduced E-cadherin expression, resulting in increased migration and invasion. These effects were reversed by miR-200b and miR-429 inhibition or overexpression. Sections of tumor xenograft model showed increased ZEB1 expression and decreased E-cadherin expression with the downregulation of 53BP1. In 18 clinical tissue samples, expression of 53BP1 was positively correlated with miR-200b and mir-429 and negatively correlated with ZEB1. It was also found that 53BP1 was associated with lymph node metastasis. Taken together, these results suggest that 53BP1 functioned as a tumor suppressor gene by its novel negative control of EMT through regulating the expression of miR-200b/429 and their target gene ZEB1.

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Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of Twist1

Cited by 32 publications

References 54 publications

Retracted: DCLK1 promotes epithelial‐mesenchymal transition via the PI3K/Akt/NF‐κB pathway in colorectal cancer

Retracted: DCLK1 promotes epithelial‐mesenchymal transition via the PI3K/Akt/NF‐κB pathway in colorectal cancer

The RNA-editing enzyme ADAR promotes lung adenocarcinoma migration and invasion by stabilizing FAK

53BP1 suppresses epithelial–mesenchymal transition by downregulating ZEB1 through microRNA‐200b/429 in breast cancer

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