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1.	Kazuo Asanoma, Emiko Hori, Sachiko Yoshida, Hiroshi Yagi, Ichiro Onoyama, Keisuke Kodama, Masafumi Yasunaga, Tatsuhiro Ohgami, Eisuke Kaneki, Kaoru Okugawa, Hideaki Yahata, Kiyoko Kato, Mutual suppression between BHLHE40/BHLHE41 and the MIR301B-MIR130B cluster is involved in epithelial-to-mesenchymal transition of endometrial cancer cells, Oncotarget, 10.18632/oncotarget.27061, 10, 45, 4640-4654, 2019.07, 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..
2.	KAZUO ASANOMA, Ge Liu, Takako Yamane, Yoko Miyanari, Tomoka Takao, Hiroshi Yagi, Tatsuhiro Ohgami, AKIMASA ICHINOE, Kenzo Sonoda, Norio Wake, Kiyoko Kato, Regulation of the Mechanism of TWIST1 Transcription by BHLHE40 and BHLHE41 in Cancer Cells, MOLECULAR AND CELLULAR BIOLOGY, 10.1128/MCB.00678-15, 35, 24, 4096-4109, 2015.12.
3.	Dan Li, Tomoka Takao, Ryosuke TSUNEMATSU, Seiichi Morokuma, Kotaro Fukushima, Hiroaki Kobayashi, Toshiaki Saito, Masutaka Furue, Norio Wake, KAZUO ASANOMA, Inhibition of AHR transcription by NF1C is affected by a single nucleotide polymorphism, and is involved in suppression of human uterine endometrial cancer, Oncogene, 30, 4950-4959, 2013.10, Involvement of the aryl hydrocarbon receptor (AHR) in carcinogenesis has been suggested in many studies. Upregulation of AHR has been reported in some cancer species, and an association between single-nucleotide polymorphisms (SNPs) of AHR and cancer risk or cancer development has also been reported. This evidence suggests the involvement of some specific SNPs in AHR transcriptional regulation in the process of carcinogenesis or cancer development, but there have been no studies to elucidate the mechanism involved. In this study, we identified the transcription factor Nuclear Factor 1-C (NF1C) as a candidate to regulate AHR transcription in a polymorphism-dependent manner. SNP rs10249788 was included in a consensus binding site for NF1C. Our results suggested that NF1C preferred the C allele to the T allele at rs10249788 for binding. Forced expression of NF1C suppressed the activity of the AHR promoter with C at rs10249788 stronger than that with T. Moreover, expression analysis of human uterine endometrial cancer (HEC) specimens showed greater upregulation of AHR and downregulation of NF1C than those of normal endometrium specimens. Sequence analysis showed HEC patients at advanced stages tended to possess T/T alleles more frequently than healthy women. We also demonstrated that NF1C suppressed proliferation, motility and invasion of HEC cells. This function was at least partially mediated by AHR. This study is the first to report that a polymorphism on the AHR regulatory region affected transcriptional regulation of the AHR gene in vitro. Because NF1C is a tumor suppressor, our new insights into AHR deregulation and its polymorphisms could reveal novel mechanisms of genetic susceptibility to cancer..
4.	Asanoma K, Kubota K, Chakraborty D, Renaud SJ, Wake N, Fukushima K, Soares MJ, Rumi MA., SATB homeobox proteins regulate trophoblast stem cell renewal and differentiation., Journal of Biological Chemistry, 287, 3, 2257-2268, 2012.01.
5.	Asanoma K, Rumi MA, Kent LN, Chakraborty D, Renaud SJ, Wake N, Lee DS, Kubota K, Soares MJ, FGF4-dependent stem cells derived from rat blastocysts differentiate along the trophoblast lineage., Developmental Biology, 351, 1, 110-119, 2011.03.
6.	Yamaguchi S, Asanoma K, Takao T, Kato K, Wake N, HOPX is epigenetically silenced in human uterine endometrial cancer and suppresses estrogen-stimulated proliferation of cancer cells by inhibiting serum response factor., International Journal of Cancer , 124, 11, 2577-2588, * equal contribution, 2009.06.
7.	Asanoma K., Kato H., Yamaguchi S., Shin C. H., Liu Z. P. Kato K., Inoue T., Miyanari Y., Yoshikawa K., Sonoda K., Fukushima K. and Wake N, HOP/NECC1, A Novel Regulator of Mouse Trophoblast Differentiation, Journal of Biological Chemistry , 282, 33, 24065-24074, 2007.07.
8.	Asanoma K, Matsuda T, Kondo H, Kato K, Kishino T, Niikawa N, Wake N, Kato H, NECC1, a candidate choriocarcinoma suppressor gene which encodes homeodomain consensus motif., Genomics, 10.1016/S0888-7543(02)00011-3, 81, 1, 15-25, 2003.01.

年度	外国語雑誌査読論文数	合計
2020年度	14	14
2019年度	12	12
2018年度	15	15
2017年度	11	11
2016年度	7	7
2015年度	3	3
2014年度	1	1
2013年度	1	1

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