Model-based Analysis of ChIP-Seq (MACS)

Zhang, Yong; Liu, Tao; Meyer, Clifford A.; Eeckhoute, Jérôme; Johnson, D. S.; Bernstein, B; Nusbaum, Chad; Myers, R; Brown, Myles; Li, Wei; Liu, X Shirley

doi:10.1186/gb-2008-9-9-r137

Cited by 15,257 publications

(13,054 citation statements)

References 13 publications

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“…This assay permits quantitative comparisons of genome-wide changes in 5-hmC levels between cell lines. Using model-based analysis of ChIP-seq (MACS) 30 , we determined global 5-hmC regions (P valueo10 À 5 , Poisson distribution, false discovery rate (FDR)o0.01; Fig. 6a) in prostate cancer cells.…”

Section: Resultsmentioning

confidence: 99%

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression

et al. 2015

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Modulation of epigenetic patterns has promising efficacy for treating cancer. 5-Hydroxymethylated cytosine (5-hmC) is an epigenetic mark potentially important in cancer. Here we report that 5-hmC is an epigenetic hallmark of prostate cancer (PCa) progression. A member of the ten-eleven translocation (TET) proteins, which catalyse the oxidation of methylated cytosine (5-mC) to 5-hmC, TET2, is repressed by androgens in PCa. Androgen receptor (AR)-mediated induction of the miR-29 family, which targets TET2, are markedly enhanced in hormone refractory PCa (HRPC) and its high expression predicts poor outcome of PCa patients. Furthermore, decreased expression of miR-29b results in reduced tumour growth and increased TET2 expression in an animal model of HRPC. Interestingly, global 5-hmC modification regulated by miR-29b represses FOXA1 activity. A reduction in 5-hmC activates PCa-related key pathways such as mTOR and AR. Thus, DNA modification directly links the TET2-dependent epigenetic pathway regulated by AR to 5-hmC-mediated tumour progression.

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Section: Resultsmentioning

confidence: 99%

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression

et al. 2015

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“…Only unique non-duplicate reads were retained. Peaks, areas where there were significantly more enriched reads mapped in the ChIP sample than the input, were determined using MACS 61 with the parameters of P value 0.00001 and false discovery rate 5%. The Bedtools software 62 was used to determine the genes closest to PBX3-binding peaks and to calculate the distance between these peaks from TSS of their closest genes.…”

Section: Discussionmentioning

confidence: 99%

PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells

Han

Zhao

et al. 2015

Nat Commun

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Tumour-initiating cells (TICs) are advocated to constitute the sustaining force to maintain and renew fully established malignancy; however, the molecular mechanisms responsible for these properties are elusive. We previously demonstrated that voltage-gated calcium channel a2d1 subunit marks hepatocellular carcinoma (HCC) TICs. Here we confirm directly that a2d1 is a HCC TIC surface marker, and identify let-7c, miR-200b, miR-222 and miR-424 as suppressors of a2d1 þ HCC TICs. Interestingly, all the four miRNAs synergistically target PBX3, which is sufficient and necessary for the acquisition and maintenance of TIC properties. Moreover, PBX3 drives an essential transcriptional programme, activating the expression of genes critical for HCC TIC stemness including CACNA2D1, EpCAM, SOX2 and NOTCH3. In addition, the expression of CACNA2D1 and PBX3 mRNA is predictive of poor prognosis for HCC patients. Collectively, our study identifies an essential signalling pathway that controls the switch of HCC TIC phenotypes.

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“…Public anti‐ZEB1 ChIP‐seq data were obtained from GEO (GSM1574278, GSM1010809, GSM803411; ENCODE Project Consortium, 2012). Peaks were called using MACS2 (Zhang et al ., 2008). cisgenome software was used to assign a binding site to the nearest gene within 50 kb of a peak (Ji et al ., 2011).…”

Section: Methodsmentioning

confidence: 99%

ZEB1‐regulated inflammatory phenotype in breast cancer cells

et al. 2017

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Zinc finger E‐box binding protein 1 (ZEB1) and ZEB2 induce epithelial‐mesenchymal transition (EMT) and enhance cancer progression. However, the global view of transcriptional regulation by ZEB1 and ZEB2 is yet to be elucidated. Here, we identified a ZEB1‐regulated inflammatory phenotype in breast cancer cells using chromatin immunoprecipitation sequencing and RNA sequencing, followed by gene set enrichment analysis (GSEA) of ZEB1‐bound genes. Knockdown of ZEB1 and/or ZEB2 resulted in the downregulation of genes encoding inflammatory cytokines related to poor prognosis in patients with cancer, including IL6 and IL8, therefore suggesting that ZEB1 and ZEB2 have similar functions in terms of the regulation of production of inflammatory cytokines. Antibody array and ELISA experiments confirmed that ZEB1 controlled the production of the IL‐6 and IL‐8 proteins. The secretory proteins regulated by ZEB1 enhanced breast cancer cell proliferation and tumor growth. ZEB1 expression in breast cancer cells also affected the growth of fibroblasts in cell culture, and the accumulation of myeloid‐derived suppressor cells in tumors in vivo. These findings provide insight into the role of ZEB1 in the progression of cancer, mediated by inflammatory cytokines, along with the initiation of EMT.

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Model-based Analysis of ChIP-Seq (MACS)

Abstract: MACS performs model-based analysis of ChIP-Seq data generated by short read sequencers.

Cited by 15,257 publications

References 13 publications

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression

PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells

ZEB1‐regulated inflammatory phenotype in breast cancer cells

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