| 1. |
Kodama Keisuke, Yahata Hidenori, Okugawa Kaoru, Tomonobe Hiroshi, Yasutake Nobuko, Yoshida Sachiko, Yagi Hiroshi, Yasunaga Masafumi, Ohgami Tatsuhiro, Onoyama Ichiro, Asanoma Kazuo, Hori Emiko, Shimokawa Mototsugu, Kato Kiyoko, Prognostic outcomes and risk factors for recurrence after laser vaporization for cervical intraepithelial neoplasia: a single-center retrospective study., International Journal of Clinical Oncology, 10.1007/s10147-020-01848-x, 26, 4, 770-776, 2021.04. |
| 2. |
Yamaguchi Shinichiro, Yahata Hideaki, Okugawa Kaoru, Kodama Keisuke, Yagi Hiroshi, Yasunaga Masafumi, Ohgami Tatsuhiro, Onoyama Ichiro, Asanoma Kazuo, Kato Kiyoko, Hypersensitivity reaction to pegylated liposomal doxorubicin administration for Mullerian carcinoma in Japanese women., Journal of Obstetrics and Gynaecology Research, 10.1111/jog.14680, 47, 4, 1544-1548, 2021.04. |
| 3. |
Yasunaga Masafumi, Yahata Hideaki, Okugawa Kaoru, Hori Emiko, Kodama Keisuke, Yagi Hiroshi, Ohgami Tatsuhiro, Onoyama Ichiro, Asanoma Kazuo, Kato Kiyoko, Prognostic impact of the subclassification of Müllerian cancer stage IV in the FIGO 2014 staging system with a focus of extra-abdominal lymph node metastases., International Journal of Clinical Oncology, 10.1007/s10147-021-01908-w, 2021.03. |
| 4. |
Kawamura Teruhiko, Tomari Hiroyuki, Onoyama Ichiro, Araki Hiromitsu, Yasunaga Masafumi, Lin Cui, Kawamura Keiko, Yokota Natsuko, Yoshida Sachiko, Yagi Hiroshi, Asanoma Kazuo, Sonoda Kenzo, Egashira Katsuko, Ito Takahiro, Kato Kiyoko, Identification of genes associated with endometrial cell ageing. , Molecular Human Reproduction, 10.1093/molehr/gaaa078, 27, 2, gaaa078, 2021.02. |
| 5. |
Yoshida Sachiko, Asanoma Kazuo, Yagi Hiroshi, Onoyama Ichiro, Hori Emiko, Matsumura Yumiko, Okugawa Kaoru, Yahata Hideaki, Kato Kiyoko, Fibronectin mediates activation of stromal fibroblasts by SPARC in endometrial cancer cells., BMC Cancer, 10.1186/s12885-021-07875-9, 21, 1, 156, 2021.02. |
| 6. |
Suzuki Izumi, Yoshida Sachiko, Tabu Kouichi, Kusunoki Soshi, Matsumura Yumiko, Izumi Hiroto, Asanoma Kazuo, Yagi Hiroshi, Onoyama Ichiro, Sonoda Kenzo, Kohno Kimitoshi, Taga Tetsuya, Itakura Atsuo, Takeda Satoru, *Kato Kato, YBX2 and cancer testis antigen 45 contribute to stemness, chemoresistance and a high degree of malignancy in human endometrial cancer., Scientific Reports, 10.1038/s41598-021-83200-5, 11, 1, 4220, 2021.02. |
| 7. |
Okugawa Kaoru, Yahata Hideaki, Sonoda Kenzo, Kodama Keisuke, Yagi Hiroshi, Ohgami Tatsuhiro, Yasunaga Masafumi, Onoyama Ichiro, Kaneki Eisuke, Asanoma Kazuo, Kobayashi Hirosaki, Kato Kiyoko, Evaluation of adjuvant chemotherapy after abdominal trachelectomy for cervical cancer: a single-institution experience., International Journal of Clinical Oncology, 10.1007/s10147-020-01778-8, 26, 1, 216-224, 2021.01. |
| 8. |
Kato Masaya, Onoyama Ichiro, Kawakami Minoru, Yoshida Sachiko, Kawamura Keiko, Kodama Keisuke, Hori Emiko, Cui Lin, Matsumura Yumiko, Yagi Hiroshi, Asanoma Kazuo, Yahata Hideaki, Itakura Atsuo, Takeda Satoru, Kato Kiyoko, Downregulation of 5-hydroxymethylcytosine is associated with the progression of cervical intraepithelial neoplasia. , PLoS One, 10.1371/journal.pone.0241482, e0241482, 2020.11. |
| 9. |
Kato Masaya, Onoyama Ichiro, Yoshida Sachiko, Cui Lin, Kawamura Keiko, Kodama Keisuke, Hori Emiko, Matsumura Yumiko, Yagi Hiroshi, Asanoma Kazuo, Yahata Hideaki, Itakura Atsuo, Takeda Satoru, Kato Kiyoko, Dual-specificity phosphatase 6 plays a critical role in the maintenance of a cancer stem-like cell phenotype in human endometrial cancer., International Journal of Cancer, 10.1002/ijc.32965, 147, 7, 1987-1999, 2020.10. |
| 10. |
Yahata Hideaki, Sonoda Kenzo, Inoue Shusaku, Yasutake Nobuko, Kodama Keisuke, Yagi Hiroshi, Yasunaga Masafumi, Ohgami Tatsuhiro, Onoyama Ichiro, Kaneki Eisuke, Okugawa Kaoru, Asanoma Kazuo, Kato Kiyoko, Is Adjuvant Therapy Necessary for Patients with Intermediate-Risk Cervical Cancer after Open Radical Hysterectomy? , Oncology, 10.1159/000508569, 98, 12, 853-858, 2020.07. |
| 11. |
Tomari Hiroyuki, Kawamura Teruhiko, Asanoma Kazuo, Egashira Katsuko, Kawamura Keiko, Honjo Ko, Nagata Yumi, Kato Kiyoko, Contribution of senescence in human endometrial stromal cells during proliferative phase to embryo receptivity. , Biology of Reproduction, 10.1093/biolre/ioaa044, 103, 1, 104-113, 2020.06. |
| 12. |
Yagi Hiroshi, Onoyama Ichiro, Asanoma Kazuo, Hori Emiko, Yasunaga Masafumi, Kodama Keisuke, Kijima Masako, Ohgami Tatsuhiro, Kaneki Eisuke, Okugawa Kaoru, Yahata Hideaki, Kato Kiyoko, Gα13-mediated LATS1 down-regulation contributes to epithelial-mesenchymal transition in ovarian cancer., FASEB Journal, 10.1096/fj.201901278R, 33, 12, 13683-13694, 2019.12. |
| 13. |
Hideaki Yahata, Kenzo Sonoda, Kaoru Okugawa, Hiroshi Yagi, Tatsuhiro Ohgami, Masafumi Yasunaga, Ichiro Onoyama, Eisuke Kaneki, Kazuo Asanoma, Kiyoko Kato, Survey of the desire to have children and engage in sexual activity after trachelectomy among young Japanese women with early-stage cervical cancer, Journal of Obstetrics and Gynaecology Research, 10.1111/jog.14099, 45, 11, 2255-2259, 2019.11, Aim: To evaluate how the desire to have children and engage in sexual activity change after trachelectomy in Japanese women with early-stage cervical cancer who strongly desired to have children before surgery. Methods: Desire to have children, coital pain, fear of sexual intercourse, sexual activity frequency and libido were assessed in cervical cancer patients who received follow-up after trachelectomy. An anonymous questionnaire survey was conducted via informed consent. Results: Of the 151 patients who underwent trachelectomy at Kyushu University Hospital between 2005 and 2015, 46 patients were evaluated; the response rate was 30%. The desire to have children disappeared in 13 of 46 (28%) patients, and 14 (30%) patients experienced increased coital pain. Moreover, 19 (41%) patients experienced fear of sexual intercourse, and sexual frequency decreased in 24 (52%) patients. Conclusion: Trachelectomy is an important fertility-sparing surgical method; however, this study revealed loss of the desire to have children and/or to engage in sexual activity in some patients after surgery. Counseling about these issues is important and should be addressed.. |
| 14. |
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.. |
| 15. |
Takako Ohmaru-Nakanishi, Kazuo Asanoma, Mai Fujikawa, Yasuyuki Fujita, Hiroshi Yagi, Ichiro Onoyama, Nobuhiro Hidaka, Kenzo Sonoda, Kiyoko Kato, Fibrosis in Preeclamptic Placentas Is Associated with Stromal Fibroblasts Activated by the Transforming Growth Factor-β1 Signaling Pathway, American Journal of Pathology, 10.1016/j.ajpath.2017.11.008, 188, 3, 683-695, 2018.03, Although fibrosis is one of the most prominent pathologic features of preeclamptic (PE) placentas, its mechanism remains largely unknown. Consistent with previous reports, we observed overexpression of collagen; actin, α2, smooth muscle, aorta; connective tissue growth factor; and fibronectin in PE placentas compared with control ones. To investigate the mechanism of fibrosis in PE placentas, placental fibroblasts were isolated from PE placentas or normal pregnancies at delivery. The expression of fibrosis-related factors in fibroblasts was evaluated by real-time RT-PCR, Western blotting, enzyme-linked immunosorbent assay, and gene microarrays. An in vitro collagen gel contraction assay was also performed. Fibroblasts isolated from PE placentas showed higher expression levels of fibrosis-related factors compared with those from control ones. Global gene expression profiling of PE fibroblasts was contrasted with that of control ones and indicated an intimate association with transforming growth factor-β1 (TGFB1) signaling. Furthermore, the PE fibroblasts expressed abundant phosphorylated SMAD family member 2 and showed higher expression levels of target genes of TGFB1 signaling compared with the control ones. The PE fibroblasts also had a greater ability to contract compared with the control ones. Contractility also depended on TGFB1 signaling. Our results suggest that TGFB1 signaling is activated in the fibroblasts in PE placentas and that these active fibroblasts contribute to fibrosis.. |
| 16. |
Shoko Kitade, Ichiro Onoyama, Hiroaki Kobayashi, Hiroshi Yagi, Sachiko Yoshida, Masaya Kato, Ryosuke Tsunematsu, Kazuo Asanoma, Kenzo Sonoda, Norio Wake, Kenichiro Hata, Keiichi I. Nakayama, Kiyoko Kato, FBXW7 is involved in the acquisition of the malignant phenotype in epithelial ovarian tumors, Cancer Science, 10.1111/cas.13026, 107, 10, 1399-1405, 2016.10, FBXW7 is a ubiquitin ligase that mediates ubiquitylation of oncoproteins, such as c-Myc, cyclin E, Notch and c-Jun. FBXW7 is a known tumor-suppressor gene, and mutations in FBXW7 have been reported in various human malignancies. In this study, we examined the sequences of the FBXW7 and p53 genes in 57 ovarian cancer clinical samples. Interestingly, we found no FBXW7 mutations associated with amino acid changes. We also investigated FBXW7 expression levels in 126 epithelial ovarian tumors. FBXW7 expression was negatively correlated with the malignant potential of ovarian tumors. That is to say, FBXW7 expression levels in ovarian cancer samples were significantly lower than those in borderline and benign tumors (P |
| 17. |
H. Yagi, K. Asanoma, T. Ohgami, A. Ichinoe, K. Sonoda, K. Kato, GEP oncogene promotes cell proliferation through YAP activation in ovarian cancer, Oncogene, 10.1038/onc.2015.505, 35, 34, 4471-4480, 2016.08, G-protein-coupled receptors (GPCRs) and their ligands function in the progression of human malignancies. G12 and G13, encoded by GNA12 and GNA13, respectively, are referred to as the GEP oncogene and are implicated in tumor progression. However, the molecular mechanisms by which G12/13 activation promotes cancer progression are not fully elucidated. Here, we demonstrate elevated expression of G12/13 in human ovarian cancer tissues. G12/13 activation did not promote cellular migration in the ovarian cancer cell lines examined. Rather, G12/13 activation promoted cell growth. We used a synthetic biology approach using chimeric G proteins and GPCRs activated solely by artificial ligands to selectively trigger signaling pathways downstream of specific G proteins. We found that G12/13 promotes proliferation of ovarian cancer cells by activating the transcriptional coactivator YAP, a critical component of the Hippo signaling pathway. Furthermore, we reveal that inhibition of YAP by short hairpin RNA or a specific inhibitor prevented the growth of ovarian cancer cells. Therefore, YAP may be a suitable therapeutic target in ovarian cancer.. |
| 18. |
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. |
| 19. |
Takako Yamane, Kazuo Asanoma, Hiroaki Kobayashi, Ge Liu, Hiroshi Yagi, Tatsuhiro Ohgami, Akimasa Ichinoe, Kenzo Sonoda, Norio Wake, Kiyoko Kato, Identification of the critical site of calponin 1 for suppression of ovarian cancer properties, Anticancer research, 35, 11, 5993-5999, 2015.11, Background: Although several studies have demonstrated the tumor suppressive function of CNN1 (calponin 1), no studies have performed a site-specific analysis of CNN1 on tumor cell activities. Materials and Methods: We herein studied the site-specific effects of CNN1 in ovarian cancer cells using full-length CNN1 (fCNN1), three CNN1 repeats (3CNRs), or the first CNN1 repeat (CNR1) expression vectors. Ovarian cancer cells stably expressing each construct were analyzed for in vitro proliferation, cell motility, invasion, and soft agar assays. An in vitro model of pleural dissemination was also established. Results: Cell proliferation, anchorageindependent colony formation, cell motility, and cell invasion were all suppressed in fCNN1, 3CNRs, and CNR1-stably-expressing cells. CNN1 expression in mesothelial cells suppressed cancer cell invasion into a monolayer of mesothelial cells. Conclusion: CNR1 showed similar suppressive effects as fCNN1. Results suggest CNR1 as a potential small synthetic peptide candidate for therapeutic strategies against ovarian cancer.. |
| 20. |
Kanako Okamoto, Ryosuke Tsunematsu, Tomoko Tahira, Kenzo Sonoda, Kazuo Asanoma, Hiroshi Yagi, Tomoko Yoneda, Kenshi Hayashi, Norio Wake, Kiyoko Kato, SNP55, a new functional polymorphism of MDM2-P2 promoter, contributes to allele-specific expression of MDM2 in endometrial cancers, BMC Medical Genetics, 10.1186/s12881-015-0216-8, 16, 1, 2015.08, Background: The functional single nucleotide polymorphism (SNP) in the MDM2 promoter region, SNP309, is known to be associated with various diseases, particularly cancer. Although many studies have been performed to demonstrate the mechanism of allele-specific expression (ASE) on SNP309, they have only utilized in vitro techniques. It is unknown whether ASE of MDM2 is ascribed solely to SNP309, in vivo. Methods: We attempted to evaluate ASE of MDM2 in vivo using post-labeling followed by automated capillary electrophoresis under single-strand conformation polymorphism conditions. For measuring a quantitative difference, we utilized the SNPs on the exons of MDM2 as markers, the status of which was heterozygous in a large population. To address the cause of ASE beyond 20 %, we confirmed sequences of both MDM2-3'UTR and promoter regions. We assessed the SNP which might be the cause of ASE using biomolecular interaction analysis and luciferase assay. Results: ASE beyond 20 % was detected in endometrial cancers, but not in cancer-free endometria samples only when an SNP rs1690916 was used as a marker. We suspected that this ASE in endometrial cancer was caused by the sequence heterogeneity in the MDM2-P2 promoter, and found a new functional polymorphism, which we labelled SNP55. There was no difference between cancer-free endometria and endometrial cancer samples neither for SNP55 genotype frequencies nor allele frequencies, and so, SNP55 alone does not affect endometrial cancer risk. The SNP55 status affected the DNA binding affinity of transcription factor Sp1 and nuclear factor kappa-B (NFκB). Transcriptional activity of the P2 promoter containing SNP55C was suppressed by NFκB p50 homodimers, but that of SNP55T was not. Only ASE-positive endometrial cancer samples displayed nuclear localization of NFκB p50. Conclusions: Our findings suggest that both the SNP55 status and the NFκB p50 activity are important in the transcriptional regulation of MDM2 in endometrial cancers.. |
| 21. |
Ge Liu, KAZUO ASANOMA, Tomoka Takao, Kiyomi Tsukimori, Uchi Hiroshi, Masutaka Furue, Kiyoko Kato, Norio Wake, Aryl hydrocarbon receptor SNP-130 C/T associates with dioxins susceptibility through regulating its receptor activity and downstream effectors including interleukin 24, TOXICOLOGY LETTERS, 10.1016/j.toxlet.2014.11.025, 232, 2, 384-392, 2015.01. |
| 22. |
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.. |
| 23. |
Tomoka Takao, KAZUO ASANOMA, Ryosuke TSUNEMATSU, Kiyoko Kato, Norio Wake, The maternally expressed gene Tssc3 regulates the expression of MASH2 transcription factor in mouse trophoblast stem cells through the AKT-Sp1 signaling pathway., Journal of Biological Chemistry, 10.1074/jbc.M112.388777, 287, 51, 42685-42694, 2012.12, Tssc3 is a maternally expressed/paternally silenced imprinted gene. Recent evidence suggests that the loss of TSSC3 results in placental overgrowth in mice. These findings showed that the TSSC3 gene functions as a negative regulator of placental growth. In this study, we describe the function of TSSC3 and its signaling pathway in mouse trophoblast stem (TS) cell differentiation. First of all, we tested Tssc3 expression levels in TS cells. TS cells expressed Tssc3, and its expression level was the highest from day 1 to 4 but was down-regulated at day 5 after the induction of differentiation. Overexpression of TSSC3 in TS cells up-regulated Gcm1 and Mash2, which are marker genes of mouse trophoblast differentiation. Down-regulation of TSSC3 by siRNA enhanced Pl1 and Tpbpa expression in TS cells cultured under stem cell conditions, suggesting the contribution of TSSC3 to the differentiation from TS to trophoblast progenitors and/or labyrinth trophoblasts. TSSC3 activated the PI3K/AKT pathway through binding with phosphatidylinositol phosphate lipids and enhanced the activity of a promoter containing an E-box structure, which is the binding sequence of the Mash2 downstream target gene promoter. PI3K inhibitor suppressed the promoter activity induced by TSSC3. TSSC3 induced Sp1 translocation from cytoplasm to nucleus through the PI3K/AKT pathway. Nuclear Sp1 activated the Mash2 transcription by Sp1 binding with a consensus Sp1-binding motif. This is the first report describing that TSSC3 plays an important role in the differentiation from TS to trophoblast progenitors and/or labyrinth trophoblasts through the TSSC3/PI3K/AKT/MASH2 signaling pathway.. |
| 24. |
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. |
| 25. |
Takao T, Asanoma K, Kato K, Fukushima K, Tsunematsu R, Hirakawa T, Matsumura S, Seki H, Takeda S, Wake N, Isolation and characterization of human trophoblast side-population (SP) cells in primary villous cytotrophoblasts and HTR-8/SVneo cell line., PLosOne, 6, 7, e21990, 2011.07. |
| 26. |
Konno T, Rempel LA, Rumi MA, Graham AR, Asanoma K, Renaud SJ, Soares MJ., Chromosome-substituted rat strains provide insights into the genetics of placentation., Physiolocgical Genomics, 43, 15, 930-941, 2011.06. |
| 27. |
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. |
| 28. |
Inoue T, Kato K, Kato H, Asanoma K, Kuboyama A, Ueoka Y, Yamaguchi S, Ohgami T, Wake N, Level of reactive oxygen species induced by p21Waf1/CIP1 is critical for the determination of cell fate., Cancer Science, 100, 7, 1275-1283, 2010.02. |
| 29. |
Kato K, Takao T, Kuboyama A, Tanaka Y, Ohgami T, Yamaguchi S, Adachi S, Yoneda T, Ueoka Y, Kato K, Hayashi S, Asanoma K, Wake N, Endometrial cancer side-population cells show prominent migration and have a potential to differentiate into the mesenchymal cell lineage., American Journal of Pathology, 176, 1, 381-392, 2010.02. |
| 30. |
*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. |
| 31. |
Tanaka Y, Kato K, Mibu R, Uchida S, Asanoma K, Hashimoto K, Nozaki M, Wake N, Medroxyprogesterone acetate inhibits proliferation of colon cancer cell lines by modulating cell cycle-related protein expression, Menopause, 15, 3, 442-453, 2008.02. |
| 32. |
Fukushima K, Murata M, Hachisuga M, Tsukimori K, Seki H, Takeda S, Asanoma K, Wake N, Hypoxia inducible factor 1 alpha regulates matrigel-induced endovascular differentiation under normoxia in a human extravillous trophoblast cell line., Placenta, 29, 4, 324-331, 2008.02. |
| 33. |
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. |
| 34. |
Kato K, Yoshimoto M, Kato K, Adachi S, Yamayoshi A, Arima T, Asanoma K, Kyo S, Nakahatat T, Wake N, Characterization of side-population cells in human normal endometrium., Human Reproduction, 22, 5, 1214-1223, 2007.05. |
| 35. |
Suga S, Kato K, Ohgami T, Yamayoshi A, Adachi S, Asanoma K, Yamaguchi S, Arima T, Kinoshita K, Wake N, An inhibitory effect on cell proliferation by blockage of the MAPK/estrogen receptor/MDM2 signal pathway in gynecologic cancer., Gycecologic Oncology, 105, 2, 341-350, 2006.05. |
| 36. |
Kato H., Inoue T., Asanoma K., Nishimura C., Matsuda T. and Wake N., Induction of human endometrial cancer cell senescence through modulation of HIF-alpha activity by EGLN1., International Journal of Cancer, 118, 5, 1144-1153, 2006.01. |
| 37. |
Kato H, Inoue T, Asanoma K, Matsuda T, Yoshikawa Y, Wake N, Activation of STAT3/5 signal pathways in complete mole and repression in choriocarcinoma cell lines., Journal of Reproductive Medicine, 51, 1, 41-48, 2006.01. |
| 38. |
Kato, H., Matsuda, T., Hirakawa, T., Ueda, K., Inoue, T., Miyanari, Y., Asanoma, K., Nakano, H. and Wake, N., Differential Diagnosis Between Complete and Partial Mole by TSSC3 Antibody Completely Correlates to DNA Diagnosis., Diagn. Mol. Pathol., 10.1097/01.pas.0000162757.91649.a3, 14, 3, 164-169, 2005.01. |
| 39. |
Asanoma K, Kato H, Inoue T, Matsuda T, Wake N, Analysis of a candidate gene associated with growth suppression of choriocarcinoma and differentiation of trophoblasts., Journal of Reproductive Medicine, 49, 8, 617-626, 2004.08. |
| 40. |
Kato, H.D., Kondoh, H., Inoue, T., Asanoma, K., Matsuda, T., Arima, T., Kato, K., Yoshikawa, T. and Wake, N., Expression of DCC and netrin-1 in normal human endometrium and its implication in endometrial carcinogenesis., Gynecol. Oncol., 10.1016/j.ygyno.2004.07.050, 95, 2, 281-289, 2004.01. |
| 41. |
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. |
| 42. |
Zhou Y, Kato H, Asanoma K, Kondo H, Arima T, Kato K, Matsuda T, Wake N, Identification of FOXC1 as a TGF-β1 responsive gene and its involvement in negative regulation of cell growth., Genomics, 10.1006/geno.2002.6860, 80, 5, 465-472, 2002.01. |
| 43. |
Kato H, Zhou Y, Asanoma K, Kondo H, Yoshikawa Y, Watanabe K, Matsuda T, Wake N and Barrett JC, Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of DCC gene., British Journal of Cancer, 10.1054/bjoc.1999.0943, 82, 2, 459-466, 2000.01. |
