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Roles of ANCO1/ANKRD11 as a Tumor Su...

Yuan, Meng,

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Roles of ANCO1/ANKRD11 as a Tumor Suppressor and Chromatin Regulator in Early-Stage Triple-Negative Breast Cancer /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Roles of ANCO1/ANKRD11 as a Tumor Suppressor and Chromatin Regulator in Early-Stage Triple-Negative Breast Cancer // Meng Yuan.
作者:	Yuan, Meng,
面頁冊數:	1 electronic resource (158 pages)
附註:	Source: Dissertations Abstracts International, Volume: 85-07, Section: B.
Contained By:	Dissertations Abstracts International85-07B.
標題:	Cellular biology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30687395
ISBN:	9798381302028

Roles of ANCO1/ANKRD11 as a Tumor Suppressor and Chromatin Regulator in Early-Stage Triple-Negative Breast Cancer /
Yuan, Meng,

Roles of ANCO1/ANKRD11 as a Tumor Suppressor and Chromatin Regulator in Early-Stage Triple-Negative Breast Cancer /Meng Yuan. - 1 electronic resource (158 pages)

Source: Dissertations Abstracts International, Volume: 85-07, Section: B.

The gene ankyrin repeat domain containing 11 (ANKRD11/ANCO1) is a putative tumor suppressor and its loss of heterozygosity and low expression levels are seen in some cancers. ANCO1 binds the oncogene amplified in breast cancer 1 (AIB1), the latter of which drives the malignant progression of breast cancer. Here we show that ANCO1 mRNA and protein expression levels are positive prognostic markers in breast cancer patients and that loss of nuclear ANCO1 protein expression predicts lower overall survival of patients with triple-negative breast cancer (TNBC). Reduction of ANCO1 expression in early-stage TNBC cells led to aneuploidy, cellular senescence, and enhanced invasion in a 3D matrix. A subpopulation of ANCO1-depleted cells enabled a collective invasion of the overall cell population in vitro and converted more rapidly to invasive lesions in a mouse xenograft tumor model. ChIP-seq analysis in ANCO1 knockdown cells showed a global increase in H3K27Ac signals that were enriched for AP-1, TEAD, STAT3 and NFκB binding motifs. ANCO1-regulated H3K27Ac peaks had a significantly higher overlap with published breast cancer enhancer peaks compared to ANCO1-independent ones. H3K27Ac engagement was associated with transcriptional activation of genes in the PI3K-AKT, EMT, and senescence pathways. In conclusion, the current study identifies the ANCO1-depleted cancer cells to be key drivers of cancer cell invasiveness. ANCO1 has hallmarks of a tumor suppressor whose loss of expression activates breast cancer-specific enhancers and oncogenic pathways that can accelerate early-stage progression of breast cancer.

English

ISBN: 9798381302028Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Tumor suppressor

Roles of ANCO1/ANKRD11 as a Tumor Suppressor and Chromatin Regulator in Early-Stage Triple-Negative Breast Cancer /
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520 $a The gene ankyrin repeat domain containing 11 (ANKRD11/ANCO1) is a putative tumor suppressor and its loss of heterozygosity and low expression levels are seen in some cancers. ANCO1 binds the oncogene amplified in breast cancer 1 (AIB1), the latter of which drives the malignant progression of breast cancer. Here we show that ANCO1 mRNA and protein expression levels are positive prognostic markers in breast cancer patients and that loss of nuclear ANCO1 protein expression predicts lower overall survival of patients with triple-negative breast cancer (TNBC). Reduction of ANCO1 expression in early-stage TNBC cells led to aneuploidy, cellular senescence, and enhanced invasion in a 3D matrix. A subpopulation of ANCO1-depleted cells enabled a collective invasion of the overall cell population in vitro and converted more rapidly to invasive lesions in a mouse xenograft tumor model. ChIP-seq analysis in ANCO1 knockdown cells showed a global increase in H3K27Ac signals that were enriched for AP-1, TEAD, STAT3 and NFκB binding motifs. ANCO1-regulated H3K27Ac peaks had a significantly higher overlap with published breast cancer enhancer peaks compared to ANCO1-independent ones. H3K27Ac engagement was associated with transcriptional activation of genes in the PI3K-AKT, EMT, and senescence pathways. In conclusion, the current study identifies the ANCO1-depleted cancer cells to be key drivers of cancer cell invasiveness. ANCO1 has hallmarks of a tumor suppressor whose loss of expression activates breast cancer-specific enhancers and oncogenic pathways that can accelerate early-stage progression of breast cancer.
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653 $a Cancer cell
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