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  1. 原著論文

Loss of the BRCA1-interacting helicase BRIP1 results in abnormal mammary acinar morphogenesis

https://repo.qst.go.jp/records/46596
https://repo.qst.go.jp/records/46596
76e1a678-7efc-4458-9828-cb2063ee83e8
Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-09-18
タイトル
タイトル Loss of the BRCA1-interacting helicase BRIP1 results in abnormal mammary acinar morphogenesis
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Daino, Kazuhiro

× Daino, Kazuhiro

WEKO 464463

Daino, Kazuhiro

Search repository
Imaoka, Tatsuhiko

× Imaoka, Tatsuhiko

WEKO 464464

Imaoka, Tatsuhiko

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Morioka, Takamitsu

× Morioka, Takamitsu

WEKO 464465

Morioka, Takamitsu

Search repository
Tani, Shusuke

× Tani, Shusuke

WEKO 464466

Tani, Shusuke

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Iizuka, Daisuke

× Iizuka, Daisuke

WEKO 464467

Iizuka, Daisuke

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Nishimura, Mayumi

× Nishimura, Mayumi

WEKO 464468

Nishimura, Mayumi

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Shimada, Yoshiya

× Shimada, Yoshiya

WEKO 464469

Shimada, Yoshiya

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臺野 和広

× 臺野 和広

WEKO 464470

en 臺野 和広

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今岡 達彦

× 今岡 達彦

WEKO 464471

en 今岡 達彦

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森岡 孝満

× 森岡 孝満

WEKO 464472

en 森岡 孝満

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谷 修祐

× 谷 修祐

WEKO 464473

en 谷 修祐

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飯塚 大輔

× 飯塚 大輔

WEKO 464474

en 飯塚 大輔

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西村 まゆみ

× 西村 まゆみ

WEKO 464475

en 西村 まゆみ

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島田 義也

× 島田 義也

WEKO 464476

en 島田 義也

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抄録
内容記述タイプ Abstract
内容記述 BRIP1 is a DNA helicase that directly interacts with the C-terminal BRCT repeat of the breast cancer susceptibility protein BRCA1 and plays an important role in BRCA1-dependent DNA repair and DNA damage-induced checkpoint control. Recent studies implicate BRIP1 as a moderate/low-penetrance breast cancer susceptibility gene. However, the phenotypic effects of BRIP1 dysfunction and its role in breast cancer tumorigenesis remain unclear. To explore the function of BRIP1 in acinar morphogenesis of mammary epithelial cells, we generated BRIP1-knockdown MCF-10A cells by shRNA-mediated RNA interference and examined its effect in a three-dimensional culture model. Genome-wide gene expression profiling by microarray and quantitative RT-PCR were performed to identify alterations in gene expression in BRIP1-knockdown cells compared with control cells. The microarray data were further investigated using the pathway analysis and Gene Set Enrichment Analysis (GSEA) for pathway identification. BRIP1 knockdown in non-malignant MCF-10A mammary epithelial cells by RNA interference induced neoplastic-like changes such as abnormal cell adhesion, increased cell proliferation, large and irregular-shaped acini, invasive growth, and defective lumen formation. Differentially expressed genes, including MCAM, COL8A1, WIPF1, RICH2, PCSK5, GAS1, SATB1, and ELF3, in BRIP1-knockdown cells compared with control cells were categorized into several functional groups, such as cell adhesion, polarity, growth, signal transduction, and developmental process. Signaling-pathway analyses showed dysregulation of multiple cellular signaling pathways, involving LPA receptor, Myc, Wnt, PI3K, PTEN as well as DNA damage response, in BRIP1-knockdown cells. Loss of BRIP1 thus disrupts normal mammary morphogenesis and causes neoplastic-like changes, possibly via dysregulating multiple cellular signaling pathways functioning in the normal development of mammary glands.
書誌情報 PLoS ONE (Online only:URL:http://www.plosone.org)

巻 8, 号 9, p. e74013, 発行日 2013-09
ISSN
収録物識別子タイプ ISSN
収録物識別子 1932-6203
DOI
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0074013
関連サイト
識別子タイプ URI
関連識別子 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0074013
関連名称 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0074013
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