The Activated Notch1 Receptor Cooperates with α-Enolase and MBP-1 in Modulating c-<i>myc</i> Activity

Hsu, Kai-Wen; Hsieh, Rong Hong; Lee, Yan-Hwa Wu; Chao, Chi-Hong; Wu, Kou Juey; Tseng, Min; Yeh, Tien Shun

doi:10.1128/mcb.00175-08

Cited by 64 publications

(73 citation statements)

References 45 publications

(58 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specific polycomb complexes, that are known to methylate H3K27, have been proposed to play a negative role in the regulation of Notch target genes [54,55]. In addition, polycomb component YY1, which is itself a DNA binding protein, has been found to be associated with NICD, to regulate c-myc promoter activity [56]. Interestingly, overexpression of the two polycomb epigenetic silencers, Pipsqueak and Lola, enhance Notch-induced overproliferation and causes hypermethylation at the Rb tumor suppressor gene [57].…”

Section: Epigenetic Regulation Of Notch Target Genesmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

567

499

View full text Add to dashboard Cite

. The Notch gene encodes a transmembrane receptor that gave the name to the evolutionary highly conserved Notch signaling cascade. It plays a pivotal role in the regulation of many fundamental cellular processes such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. After specific ligand binding, the intracellular part of the Notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor RBP-J. In the absence of activated Notch, RBP-J represses Notch target genes by recruiting a corepressor complex. Here, we review Notch signaling with a focus on gene regulatory events at Notch target genes. This is of utmost importance to understand Notch signaling since certain RBP-J associated cofactors and particular epigenetic marks determine the specificity of Notch target gene expression in different cell types. We subsequently summarize the current knowledge about Notch target genes and the physiological significance of Notch signaling in development and cancer.

show abstract

Section: Epigenetic Regulation Of Notch Target Genesmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

567

499

View full text Add to dashboard Cite

show abstract

“…Both pcDNA-HA-MBP-1 and pcDNA-HA-␣-enolase expression constructs contain cDNAs of MBP-1 and ␣-enolase with N-terminal HA tags (Hsu et al, 2008). The fusion protein plasmids pcDNA-HA-MBP-1 (1-178), pcDNA-HA- , and pcDNA-HA-MBP-1 (232-338) direct the expression of HA-fusion proteins with amino acid residues 1-178, 190-338, and 232-338 of MBP-1, respectively.…”

Section: Plasmids and Plasmid Constructionmentioning

confidence: 99%

“…As Hsu et al described previously (Hsu et al, 2008), 4000 parental cells (SC-M1, AGS, AZ521, NUGC-3, and KATO III cells) and 8000 SC-M1/ pcDNA3 or SC-M1/HA-MBP-1 cells were used for assay of anchorage-independent growth in soft agar. Then cells were incubated at 37°C for 14 d and 200 l of medium was added every 3 d to prevent desiccation.…”

Section: Colony-forming Assaymentioning

confidence: 99%

“…The pcDNA-COX-2 contains cDNA of human COX-2 (Su et al, 2004). The siRNA vectors were constructed in pLKO.1 siRNA vector to knockdown the endogenous MBP-1 and ␣-enolase (#22 and #24) (Hsu et al, 2008). The pLKO.1-shLuc siRNA vector against luciferase was a control for knockdown validation in this study.…”

mentioning

confidence: 99%

“…The 210-base pairs DNA fragment of c-Myc promoter was amplified with primers 5Ј-GAGGAGCAGCAGAGAAAGG-3Ј and 5Ј-TCCCCCACGCCCTCTGC-3Ј. Furthermore, percentages of immunoprecipitated promoter fragments were quantified by real-time PCR using SYBR green as described elsewhere (Hsu et al, 2008) and normalized to total input DNA. …”

mentioning

confidence: 99%

See 2 more Smart Citations

MBP-1 Suppresses Growth and Metastasis of Gastric Cancer Cells through COX-2

Hsu

Hsieh

et al. 2009

MBoC

Self Cite

View full text Add to dashboard Cite

INTRODUCTIONGastric cancer is one of the most frequent neoplasms and leading causes of cancer-related mortality worldwide (Terry et al., 2002;Executive Yuan, 2006). At present, curative surgery of its primary tumor and control of lymph node metastasis are still the mainstay of treatment for gastric cancer without distant metastasis . However, gastric cancer with distant metastasis remains incurable now. More than 95% of malignancies of the stomach are adenocarcinomas (Smith et al., 2006). The risk factors of human gastric cancer include diet, Helicobacter pylori infection, and accumulation of specific genetic alterations (Gonzalez et al., 2002;Ushijima and Sasako, 2004;Zheng et al., 2004). To date, the regulatory mechanism of aggressiveness in gastric cancer has not yet been clearly characterized. Therefore, it is essential to gain further insights into the physiology of gastric cancer and its accumulated genetic alterations.The inducible cyclooxygenase, COX-2, catalyzes the ratelimiting step in conversion of arachidonate into prostaglandin E 2 (PGE 2 ). It was shown that COX-2 expression is upregulated in gastric cancer (Ristimäki et al., 1997;Uefuji et al., 1998;Yamamoto et al., 1999;Lim et al., 2000). COX-2 expression is also correlated with depth of invasion, lymphatic vessel invasion, lymph node metastasis, and poor prognosis of human gastric carcinoma (Murata et al., 1999;Ohno et al., 2001;Shi et al., 2003;Chen et al., 2006). Epithelial-mesenchymal transition (EMT) plays a key role in development and tumorigenesis (for a review, see Thiery and Sleeman, 2006). In gastric cancer cells with fibroblastoid morphological changes, EMT signaling was suggested to promote motility and invasiveness through decreasing cell-cell adhesion (Katoh, 2005). Recently, COX-2 expression was found to enhance EMT stimulated by TGF-␤ through a PGE 2 -dependent manner in breast cancer (Neil et al., 2008). In this scenario, the induction of COX-2 expression in gastric cancer could further induce EMT to promote metastasis.The c-Myc promoter binding protein 1 (MBP-1), a negative regulator of c-myc expression, is ubiquitously expressed in normal human tissues (Ray et al., 1994 groove of the major c-Myc promoter, the P2 promoter (Chaudhary and Miller, 1995). The 37-kDa MBP-1 is produced by alternative translation initiation from ␣-enolase gene but without enzyme activity of enolase (Feo et al., 2000;Subramanian and Miller, 2000). So far, several MBP-1-associating proteins were identified, including histone deacetylase HDAC1 (Ghosh et al., 1999), MIP2A/sedlin (Ghosh et al., 2001), MEK5␣ (Ghosh et al., 2005a), NS1-BP (Perconti et al., 2007), and Notch1 receptor intracellular domain (Hsu et al., 2008). The downstream target genes of MBP-1 remain unclear exclusive of c-myc. It was reported that MBP-1 could regulate target genes at least through p53-p21 pathway (Ghosh et al., 2008). Mounting evidence indicates that both MBP-1 and ␣-enolase are involved in tumorigenesis of breast carcinoma (Ray et al., 1995), nonsmall cell lung cancer (Chan...

show abstract

ER stress‐related ATF6 upregulates CIP2A and contributes to poor prognosis of colon cancer

et al. 2018

View full text Add to dashboard Cite

Endoplasmic reticulum (ER) stress is an adaptive response to various stress conditions and plays emerging roles in cancer. Activating transcription factor 6 (ATF6), one of the three major ER stress transducers, has been shown to contribute to chemoresistance by altering cancer cell survival. Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an oncogene, and its expression has been correlated with the prognosis of patients with cancer. In this study, we aimed to explore the relationship between ER stress‐related ATF signaling and CIP2A. We found that CIP2A expression was positively correlated with ATF6 expression by analyzing publicly available RNA sequence data of patients with colorectal cancer (The Cancer Genome Atlas, TCGA). In addition, we demonstrated that tunicamycin‐induced ER stress in vitro upregulated ATF6 and CIP2A. Mechanistically, we found that ATF6 directly bound to the CIP2A promoter and induced CIP2A gene expression, which contributed to colon cancer cell survival. Furthermore, knockdown of CIP2A reduced the viability of cells under ER stress. Most importantly, immunohistochemical analysis of a tissue microarray from a colon cancer patient cohort showed that higher expression levels of ATF6 and CIP2A were associated with a trend toward poor prognosis. Taken together, our results show that ER stress‐related ATF6 upregulates CIP2A and contributes to the prognosis of colon cancer. Targeting CIP2A may disrupt ER stress‐mediated colon cancer cell survival and thus improve the prognosis of patients with colon cancer.

show abstract

The Activated Notch1 Receptor Cooperates with α-Enolase and MBP-1 in Modulating c-myc Activity

Cited by 64 publications

References 45 publications

The Notch signaling pathway: Transcriptional regulation at Notch target genes

The Notch signaling pathway: Transcriptional regulation at Notch target genes

MBP-1 Suppresses Growth and Metastasis of Gastric Cancer Cells through COX-2

ER stress‐related ATF6 upregulates CIP2A and contributes to poor prognosis of colon cancer

Contact Info

Product

Resources

About