Overexpression of Pofut1 and activated Notch1 may be associated with poor prognosis in breast cancer

Wan, Guo‐Xing; Lin, Tian; Yu, Yuandong; Li, Fang; Wang, Xuanbin; Li, Chen; Shou-heng, Deng; Yu, Xuanji; Cai, Xiaojun; Zuo, Zhuang; Cao, Fengjun

doi:10.1016/j.bbrc.2017.07.053

Cited by 30 publications

(25 citation statements)

References 19 publications

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“…Six of the top ten Over-UpT genes in Chr20 have been involved in tumorigenesis based on overexpression, functional assays and clinical data: CSE1L 44 , 45 , POFUT1 54 , TPX2 55 RPN2 56 , PLCB4 57 , CPNE1 58 , 59 .…”

Section: Resultsmentioning

confidence: 99%

“…We are not suggesting that Over-UpT are cancer driver genes, but that this class of transcripts can be prioritized for further functional studies on such specific type of cancer genes (BCNA-associated). Indeed, the list of Over-UpT genes in Chr20, ranked according to overexpression, shows in the top positions several bona fide cancer driver genes, already implicated in cancer pathogenesis on the basis of evidence at the protein, functional and clinical level 44 , 45 , 54 – 59 , 62 . Moreover, it should be kept in mind that transcript level changes are not necessarily translated in phenotypic effects and several downstream mechanisms can counterbalance such modifications 63 , 64 .…”

Section: Discussionmentioning

confidence: 99%

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Positive Caricature Transcriptomic Effects Associated with Broad Genomic Aberrations in Colorectal Cancer

Condorelli

Spampinato

Valenti

et al. 2018

Sci Rep

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We re-examined the correlation between Broad Genomic Aberrations (BGAs) and transcriptomic profiles in Colorectal Cancer (CRC). Two types of BGAs have been examined: Broad Copy-Number Abnormal regions (BCNAs), distinguished in gain- and loss-type, and Copy-Neutral Loss of Heterozygosities (CNLOHs). Transcripts are classified as “OverT” or “UnderT” if overexpressed or underexpressed comparing CRCs bearing a specific BGA to CRCs not bearing it and as “UpT” or “DownT” if upregulated or downregulated in cancer compared to normal tissue. BGA-associated effects were evaluated by changes in the “Chromosomal Distribution Index” (CDI) of different transcript classes. Data show that UpT are more sensitive than DownT to BCNA-associated gene dosage effects. “Over-UpT” genes are upregulated in cancer and further overexpressed by gene dosage, defining the so called “positive caricature transcriptomic effect”. When Over-UpT genes are ranked according to overexpression, top positions are occupied by genes implicated at the functional and therapeutic level in CRC. We show that cancer-upregulated transcripts are sensitive markers of BCNA-induced effects and suggest that analysis of positive caricature transcriptomic effects can provide clues toward the identification of BCNA-associated cancer driver genes.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Positive Caricature Transcriptomic Effects Associated with Broad Genomic Aberrations in Colorectal Cancer

Condorelli

Spampinato

Valenti

et al. 2018

Sci Rep

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“…The patients did not receive any anti-tumor therapy before surgery. All samples were pathologically diagnosed based on the World Health Organization (WHO) classification 17 , and were referred to the protocol approved by the Ethical Committee of the Nantong Tumor Hospital.…”

Section: Methodsmentioning

confidence: 99%

SIRT1 promotes formation of breast cancer through modulating Akt activity

Jin¹,

Wei²,

Xu³

et al. 2018

J. Cancer

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The silent information regulation factor 1 (sirtuin Type 1, SIRT1), as a kind of NAD+ dependent class III histone deacetylation enzyme, has been found to be involved in tumor proliferation, invasion, and metastasis. The roles of SIRTl in breast cancer is multifaceted depending on its substrate from upstream or downstream signaling pathway. In this study, we sought to make clear the regulating effects of SIRT1 in breast cancer cells, and to explore the underlying mechanisms through which SIRT1 regulates breast cancer. First, our results showed that SIRT1 was significantly up-regulated in breast cancer tissues and cells, which correlated with histological grade, tumor size, as well as lymph node metastasis. Then we established SIRT1-overexpressed and SIRT1- knockdown breast cancer cell lines to investigate the functions of SIRT1 in regulating colony formation, cell proliferation, cell cycle, cell apoptosis and migration. We found that overexpression of SIRT1 significantly promoted breast cancer growth both in vitro and in vivo, whereas knockdown of SIRT1 inhibited these phenotypes. Furthermore, SIRT1 was found to interact with Akt directly, consequently promoting the activity of Akt in breast cancer cells in vitro and positively correlating with expression of Akt, P-Akt, in breast cancer tissues in vivo. Down regulation the activity of Akt partially weakened the proliferative effect mediated by SIRT1. Taken together, our results demonstrated SIRT1's tumor promotion function and potential mechanisms in breast cancer, thus providing valuable therapeutic targets for breast cancer.

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“…Elevated levels of NR1 and NR4 were reported in the early breast cancer lesions, ductal carcinoma in situ (DCIS), and the triple negative breast cancer tumors [205,206]. Elevated levels of NR1 and JAG1 were correlated with poor patient prognosis, and shorter disease-free survival [207][208][209][210][211][212]. Although NR3 gene amplification was observed in breast cancer specimens at a low frequency [213], higher expression of NR3 was associated with improved recurrence-free survival in luminal A, luminal B and basal-like subtypes of breast cancers except for the HER2 overexpressing subtype [88].…”

Section: Notch Signaling In Breast Carcinogenesismentioning

confidence: 99%

Notch-Induced Expression of FZD7 Requires Noncanonical NOTCH3 Signaling in Human Breast Epithelial Cells

Bhat

Sun

Weger

et al. 2016

Stem Cells and Development

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The evolutionarily conserved Notch and Wnt signaling pathways have demonstrated roles in normal mammary gland development and in breast carcinogenesis. We previously reported that in human mammary gland, signaling through NOTCH3 alone regulates the commitment of the undifferentiated bipotential progenitors to the luminal cell fate, indicating that NOTCH3 may regulate the expression of unique genes apart from the other Notch receptors. In this study, we used gain of function and loss of function experiments and found that a Wnt signaling receptor, Frizzled7 (FZD7), is a unique and nonredundant target of NOTCH3 in human breast epithelial cells. Interestingly, neither the constitutively active forms of NOTCH1-2, 4 nor loss of expression of these receptors were able to alter expression of FZD7 in human breast epithelial cells. We further show that FZD7-expressing cells are found more frequently in the luminal progenitor-enriched subpopulation of cells obtained from breast reduction samples compared with the undifferentiated bipotent progenitors. Also, we show that NOTCH3-induced expression of FZD7 occurs in the absence of CSL (CBF1-Suppressor of Hairless-Lag-1). Our data suggest that noncanonical Notch signaling through NOTCH3 could modulate Wnt signaling via FZD7 and in this way, might be involved in luminal cell differentiation.

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Overexpression of Pofut1 and activated Notch1 may be associated with poor prognosis in breast cancer

Cited by 30 publications

References 19 publications

Positive Caricature Transcriptomic Effects Associated with Broad Genomic Aberrations in Colorectal Cancer

Positive Caricature Transcriptomic Effects Associated with Broad Genomic Aberrations in Colorectal Cancer

SIRT1 promotes formation of breast cancer through modulating Akt activity

Notch-Induced Expression of FZD7 Requires Noncanonical NOTCH3 Signaling in Human Breast Epithelial Cells

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