抄録
BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors involved in multiple cell activities including epithelial-to-mesenchymal transition (EMT). However, the expression mechanism of BHLHE40/41 in EMT remains unclear. In the present study, we showed that the expression levels of BHLHE40/41 were negatively correlated with those of the microRNA (MIR) 130 family in endometrial cancer (EC) specimens. Our in vitro assays indicated that the expression of BHLHE40/41 was suppressed directly by the MIR130 family in a 3'-untranslated region-mediated manner. In EC cells, the MIR130 family promoted EMT and tumor cell invasion by suppressing the expression of BHLHE40/41. We identified the critical promoter region of the MIR301B-MIR130B cluster for its basal transcription by the transcription factor, SP1. We also found that BHLHE40/41 suppressed the expression of MIR301B and MIR130B, and we identified a binding site in the promoter region for BHLHE40/41. This study is the first to report that BHLHE40/41 and the MIR301B-MIR130B cluster suppressed each other to regulate EMT and invasion of EC cells. We propose that BHLHE40/41 and the MIR130 family are excellent markers to predict the progression of EC cases, and that molecular therapy targeting the MIR130 family-BHLHE40/41 axis may effectively control EC extension.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 4640-4654 |
| ページ数 | 15 |
| ジャーナル | Oncotarget |
| 巻 | 10 |
| 発行部数 | 45 |
| 出版物ステータス | 出版済み - 1 1 2019 |
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All Science Journal Classification (ASJC) codes
- Oncology
これを引用
Mutual suppression between BHLHE40/BHLHE41 and the MIR301B-MIR130B cluster is involved in epithelial-to-mesenchymal transition of endometrial cancer cells. / Asanoma, Kazuo; Hori, Emiko; Yoshida, Sachiko; yagi, hiroshi; Onoyama, Ichiro; Kodama, Keisuke; Yasunaga, Masafumi; Ogami, Tatsuhiro; Eisuke, Kaneki; Kaoru, Okugawa; Yahata, Hideaki; Kato, Kiyoko.
：: Oncotarget, 巻 10, 番号 45, 01.01.2019, p. 4640-4654.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Mutual suppression between BHLHE40/BHLHE41 and the MIR301B-MIR130B cluster is involved in epithelial-to-mesenchymal transition of endometrial cancer cells
AU - Asanoma, Kazuo
AU - Hori, Emiko
AU - Yoshida, Sachiko
AU - yagi, hiroshi
AU - Onoyama, Ichiro
AU - Kodama, Keisuke
AU - Yasunaga, Masafumi
AU - Ogami, Tatsuhiro
AU - Eisuke, Kaneki
AU - Kaoru, Okugawa
AU - Yahata, Hideaki
AU - Kato, Kiyoko
PY - 2019/1/1
Y1 - 2019/1/1
N2 - BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors involved in multiple cell activities including epithelial-to-mesenchymal transition (EMT). However, the expression mechanism of BHLHE40/41 in EMT remains unclear. In the present study, we showed that the expression levels of BHLHE40/41 were negatively correlated with those of the microRNA (MIR) 130 family in endometrial cancer (EC) specimens. Our in vitro assays indicated that the expression of BHLHE40/41 was suppressed directly by the MIR130 family in a 3'-untranslated region-mediated manner. In EC cells, the MIR130 family promoted EMT and tumor cell invasion by suppressing the expression of BHLHE40/41. We identified the critical promoter region of the MIR301B-MIR130B cluster for its basal transcription by the transcription factor, SP1. We also found that BHLHE40/41 suppressed the expression of MIR301B and MIR130B, and we identified a binding site in the promoter region for BHLHE40/41. This study is the first to report that BHLHE40/41 and the MIR301B-MIR130B cluster suppressed each other to regulate EMT and invasion of EC cells. We propose that BHLHE40/41 and the MIR130 family are excellent markers to predict the progression of EC cases, and that molecular therapy targeting the MIR130 family-BHLHE40/41 axis may effectively control EC extension.
AB - BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors involved in multiple cell activities including epithelial-to-mesenchymal transition (EMT). However, the expression mechanism of BHLHE40/41 in EMT remains unclear. In the present study, we showed that the expression levels of BHLHE40/41 were negatively correlated with those of the microRNA (MIR) 130 family in endometrial cancer (EC) specimens. Our in vitro assays indicated that the expression of BHLHE40/41 was suppressed directly by the MIR130 family in a 3'-untranslated region-mediated manner. In EC cells, the MIR130 family promoted EMT and tumor cell invasion by suppressing the expression of BHLHE40/41. We identified the critical promoter region of the MIR301B-MIR130B cluster for its basal transcription by the transcription factor, SP1. We also found that BHLHE40/41 suppressed the expression of MIR301B and MIR130B, and we identified a binding site in the promoter region for BHLHE40/41. This study is the first to report that BHLHE40/41 and the MIR301B-MIR130B cluster suppressed each other to regulate EMT and invasion of EC cells. We propose that BHLHE40/41 and the MIR130 family are excellent markers to predict the progression of EC cases, and that molecular therapy targeting the MIR130 family-BHLHE40/41 axis may effectively control EC extension.
UR - http://www.scopus.com/inward/record.url?scp=85070793167&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85070793167&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:85070793167
VL - 10
SP - 4640
EP - 4654
JO - Oncotarget
JF - Oncotarget
SN - 1949-2553
IS - 45
ER -