Researchers Database

sakamoto takako

    EnviromentalandPreventiveMedicine Assistant Professor
Last Updated :2021/11/23

Researcher Information

URL

J-Global ID

Research Interests

  • 植物エストロゲン   乳がん   腫瘍微小環境   レスベラトロール   エストロゲンレセプター   ホルモン依存性がん   エストロゲン   p53   細胞内情報伝達   

Research Areas

  • Life sciences / Hygiene and public health (non-laboratory)
  • Life sciences / Hygiene and public health (laboratory)
  • Life sciences / Hygiene and public health (non-laboratory)
  • Life sciences / Hygiene and public health (laboratory)
  • Life sciences / Tumor biology

Academic & Professional Experience

  • 2005/09 - Today  Jichi Medical UniversitySchool of Medicine講師

Published Papers

  • Hyogo Horiguchi, Etsuko Oguma, Takako Sakamoto, Katsuyuki Murata, Fujio Kayama
    ARCHIVES OF TOXICOLOGY 88 (1) 137 - 144 0340-5761 2014/01 [Refereed][Not invited]
     
    Diethylstilbestrol is an estrogenic endocrine disrupter that has diverse health effects in humans. Bisphenol A is another estrogen-like chemical with possible similar effects to diethylstilbestrol, which has been increasingly used for industry to lead to globally widespread human exposure to it. Hematopoiesis is another of their possible targets, since estrogen suppresses erythropoietin induction to induce anemia. The aim of this study was to clarify the effects of diethylstilbestrol and bisphenol A on erythropoietin induction in rats. We observed the effects of one-shot subcutaneous injection of diethylstilbestrol or bisphenol A on hypoxia-, bleeding-, and cobalt-stimulated erythropoietin induction within 24 h and the hematological outcomes after repeated subcutaneous injection of diethylstilbestrol three times a week for 1 month in rats. Diethylstilbestrol at 10-1,000 mu g/kg suppressed stimulus-elevated levels of plasma erythropoietin and its renal mRNA induction. In contrast, bisphenol A at 1,000 mu g/kg did not suppress plasma erythropoietin elevated by any stimuli. Repeated injection of diethylstilbestrol at 1,000 mu g/kg to rats for 1 month induced an anemic trend due to decelerated erythropoiesis through the insufficient production of erythropoietin, mimicking the effects of estradiol. In conclusion, diethylstilbestrol has a suppressive effect on erythropoietin induction, leading to deceleration of erythropoiesis and the development of anemia.
  • Takako Sakamoto, Hyogo Horiguchi, Etsuko Oguma, Fujio Kayama
    JOURNAL OF NUTRITIONAL BIOCHEMISTRY 21 (9) 856 - 864 0955-2863 2010/09 [Refereed][Not invited]
     
    Phytoestrogens have attracted attention as being safer alternatives to hormone replacement therapy (HRT) and as chemopreventive reagents for breast cancer because dietary soy isoflavone intake has been correlated with reduction in risk. To identify safe and effective phytoestrogen candidates for HRT and breast cancer prevention, we investigated the effects of daidzein, genistein, coumestrol, resveratrol and glycitein on cell growth, cell cycle, cyclin D1 expression, apoptosis, Bcl-2/Bax expression ratio and p53-dependent or NF-kappa B-dependent transcriptional activity in MCF-7 breast cancer cells. Phytoestrogens, except for glycitein, significantly enhanced estrogen-response-element-dependent transcriptional activity up to a level similar to that of 17 beta-estradiol (E(2)) E(2) increased cell growth significantly, coumestrol Increased cell growth moderately, and resveratrol and glycitein reduced cell growth. Phytoestrogens, except for glycitein, stimulated the promotion of cells to G(1)/S transition in cell cycle analysis, similar to E(2). This stimulation was accompanied by transient up-regulation of cyclin D1. While genistein, resveratrol and glycitein all increased apoptosis and reduced the Bcl-2/Bax ratio, resveratrol reduced this ratio more than either genistein or glycitein Moreover, resveratrol significantly enhanced p53-dependent transcriptional activity, but slightly reduced NF-kappa B-dependent transcriptional activity On knockdown analysis, genistein, resveratrol and glycitein all reduced the Bcl-2/Bax ratio in the presence of apoptosis-inducing stimuli, and estrogen receptor (ER) a silencing had no effect on these reductions. In contrast, in the absence of apoptosis-inducing stimuli, only resveratrol reduced the ratio, and ER alpha silencing abolished this reduction Thus, resveratrol might be the most promising candidate for HRT and chemoprevention of breast cancer due to its estrogenic activity and high antitumor activity (C) 2010 Elsevier Inc. All rights reserved
  • S Hayashi, T Sakamoto, A Inoue, N Yoshida, Y Omoto, Y Yamaguchi
    JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY 86 (3-5) 433 - 442 0960-0760 2003/09 [Not refereed][Invited]
     
    Estrogen and its receptor play important roles in genesis and malignant progression of estrogen-dependent cancers, together with various growth factors. Functional cross-talk between estrogen-signaling and growth factor-mediated signaling pathways has been reported. Firstly, we show an example of the cross-talk that may alter the effect of antagonist on the breast and endometrial cancer cell growth. Our observations suggest that the constitutively activated MAP kinase-signaling pathway in endometrial cancer cells might enhance the transcriptional activity of ERalpha via phosphorylation of AF-1 domain. This mechanism may cause the growth stimulative effect of tamoxifen on the endometrium. Secondly, we show our recent study for comprehensive understanding of estrogen-signaling pathway using cDNA microarray. According to the results of the expression profiling of estrogen-responsive genes in ER-positive breast cancer cells using large-scale cDNA microarray, the custom-made cDNA microarray, on which only estrogen-responsive genes were loaded, was produced. Using this microarray consisting of the narrowed gene subset, we analyzed estrogen responsiveness of various cell lines and effect of estrogen antagonists. Aim of this study is not only to address the molecular mechanisms of estrogen-dependent growth of breast cancer, but also to develop the new diagnostic tools for responsiveness to hormone therapy of primary breast cancer patients. Finally, in order to understand the local tumor biology including stroma-cancer interaction, we recently developed the new analytical system using ERE-GFP introduced into breast cancer cells. Several observations indicated that these reporter cells were useful for assessment of stimulative effects of stroma cells adjacent to breast cancer on the estrogen- signaling pathway. These studies may provide not only new clues for elucidation of the molecular mechanisms of estrogen-dependent growth of breast cancer, but also assessment of anti-estrogen responses of individual breast cancer for patient-tailored hormone therapy. (C) 2003 Elsevier Ltd. All rights reserved.
  • T Sakamoto, H Eguchi, Y Omoto, T Ayabe, H Mori, S Hayashi
    MOLECULAR AND CELLULAR ENDOCRINOLOGY 192 (1-2) 93 - 104 0303-7207 2002/06 [Refereed][Not invited]
     
    Tamoxifen is an estrogen receptor (ER)-antagonist that is widely used for the treatment of breast cancer, although it increases the risk of endometrial cancer. The mechanism mediating the stimulatory effect of tamoxifen on endometrial cancer is presently unknown. In this study we examined the effects of tamoxifen on Ishikawa 3H-12 endometrial cancer cells and MCF-7 breast cancer cells. Ishikawa cell growth was stimulated by 4-hydroxytamoxifen and accompanied by increased transcriptional activity of the endogenous ER. These stimulatory effects did not occur in MCF-7 cells. The relative transcriptional activity of the activation function (AF) I domain of ERalpha compared with that of the AF2 domain was 4-fold higher in Ishikawa cells than in MCF-7 cells, Mitogen-activated protein (MAP) kinase, which stimulates the transcriptional activity of AF1, was constitutively activated in Ishikawa cells, but not in MCF-7 cells. These observations suggest that the constitutively activated MAP kinase-signaling pathway in Ishikawa cells enhances the transcriptional activity of ERalpha via the AF1 domain. This ERalpha activation pathway may be involved in the stimulatory effect of tamoxifen on the development and/or progression of endometrial cancer. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
  • T Sakamoto, T Murase, H Urushibata, K Kato, H Takada, T Imamura, H Mori, N Wake
    GYNECOLOGIC ONCOLOGY 71 (1) 53 - 58 0090-8258 1998/10 [Refereed][Not invited]
     
    Recently, microsatellite instability (MI) has been demonstrated in some types of human cancers. In this study, we attempted to determine the frequency of MI in endometrial cancers and evaluate whether replication error (RER)-positive phenotype is correlated with known genetic mutations or the aberrations of other pathways in endometrial cancers. Seventy-two primary endometrial cancers were examined for microsatellite instability. Eleven tumors (15%) had RERs at two or more microsatellite loci, suggesting that generalized MI may be a molecular manifestation of endometrial cancers. We next examined whether the MI was associated with changes in the K-ras protooncogene, p53 tumor suppressor gene, and 18q LOH, which were frequently detected in endometrial cancers. The MI did not confer the potential to produce point mutations in the K-ras gene or 18q LOH, whereas the data were insufficient to identify the correlation between MI and p53 mutations in the cancers. These results suggest the presence of multiple mutation subsets that act in a complementary fashion in endometrial cancer development. (C) 1998 Academic Press.
  • Kato K, Sakamoto T, Wake N
    Oncology 55(Suppl 1) 41 - 48 1998 [Not refereed][Invited]
  • T Sakamoto, N Nomura, H Mori, N Wake
    GYNECOLOGIC ONCOLOGY 63 (2) 173 - 179 0090-8258 1996/11 [Refereed][Not invited]
     
    To define the target of chromosome 17p deletions, allelic losses in the 17p11.2 to 13.3 regions of 32 ovarian cancers were investigated. Twenty-one (68%) of 31 informative cancers had deletions on chromosome 17p. None of these 21 cancers involved deletions in the entire chromosome 17p even if deletions of a small chromosome region were infrequent, Of these 21, 17 cancers contained deletions at 17p13.1 or neighboring regions, The remaining 4 cancers with 17p deletions were uninformative for deletions at 17p13.1. Thus, most 17p deletions seemed to target the 17p13.1 region in ovarian cancers, Of the 30 ovarian cancers screened, 6 contained p53 mutations. One p53 allele was lost as a consequence of deletion and the other was mutated in 4 cancers, Seventeen cancers with deletions on 17p showed no evidence of p53 mutations, Thus, deletions on 17p that are common in ovarian cancers are not always accompanied by p53 gene mutations. (C) 1996 Academic Press, Inc.
  • Accumulation of genetic events in endometrial carcinoma and its cell growth inhibition by antisense oligonucleotide complementary to the mutated K-ras gene.
    Wake N, Gima T, Nishida J, Arima T, Imamura T, Nishida M, Kato K, Matsuda T, Tamura T, Hachiya T, Sakamoto T, Oshimura M
    Cancer Mol. Biol. 1 145 - 156 1994 [Not refereed][Invited]
  • Tatsuo Yamamoto, Sachiko Yoshimura, Yukifumi Sasamori, Takako Sakamoto, Masahiro Ogino, Akira Kambegawa, Shouichi Okinaga, Kiyoshi Arai
    Asia‐Oceania Journal of Obstetrics and Gynaecology 18 (2) 177 - 185 1447-0756 1992 [Refereed][Not invited]
     
    In order to investigate the renal change in preeclampsia, molecular weight and specific protein analyses in unconcentrated urine were performed by the immunoblot method. Urine samples were taken from 34 preeclamptic cases (pure type), including 20 severe cases. Polypeptide profiles of urine consisted of four patterns: low MW (L) pattern (tubular damage), high MW (H) pattern (glomerular damage), high and low MW (HL) pattern, and middle MW (M) pattern. The incidences of the HL, H, L, and M patterns were 26.5%, 14.7%, 11.8%, and 47.1%, respectively. The HL pattern was found more frequently in severe proteinuria than in mild proteinuria. High incidences of the HL and H patterns were found in the hypertensive group. Larger amounts of IgM, fibronection, IgG, and β2 microglobulin in urine were confirmed using specific antibodies. Our results suggest that the immunoblot method makes it possible to differentiate glomerular and tubular damages and to evaluate the severity of renal damage in preeclampsia using unconcentrated urine. © 1992 Japanese Society of Obstetrics and Gynaecology
  • M OGINO, T SAKAMOTO, T YAMAMOTO, H MORI, S OKINAGA, K ARAI
    GYNECOLOGIC ONCOLOGY 38 (1) 32 - 36 0090-8258 1990/07 [Refereed][Not invited]

MISC

  • 坂本 隆子, 江口 英孝, 森 宏之, 林 慎一  ホルモンと臨牀  51-  210  -214  2003/03  [Not refereed][Not invited]
  • T. Sakamoto, M. Ogino, T. Yamamoto, H. Mori, S. Okinaga, T. Sonoda, K. Ueda, S. I. Obi, T. Kobayashi  Acta Obstetrica et Gynaecologica Japonica  45-  (5)  457  -463  1993  [Not refereed][Not invited]
     
    Twenty-one human ovarian epithelial carcinomas (13 serous, 3 mucinous, 2 endometrioid and 3 clear cell type) were examined for allelic losses of p53 tumor suppressor gene, pYNZ22 or pTHH59 on chromosome 17. High-molecular-weight DNA was extracted from ovarian tumor tissues and normal ones obtained from the same patients, and was subjected to Southern blot analysis. The filters were hybridized with p53 cDNA probe or two VNTR probes on chromosome 17 (pYNZ22, pTHH59). By comparing the hybridized band pattern of the normal tissue with that of the tumor, loss of heterozygosity (LOH) was detected. Frequent LOHs were detected in 5 of 14 informative cases (36%) on p53 and in 9 of 20 (45%) on pYNZ22, but LOH on pTHH59 was observed less frequently than those of p53 and pYNZ22 (one of 7 cases : 14%). These results suggest that allelic loss of p53 may play an important role in the development and/or progression of ovarian carcinomas.
  • T. Sakamoto, M. Ogino, T. Yamamoto, H. Mori, S. Okinaga, K. Arai  Acta Obstetrica et Gynaecologica Japonica  42-  (5)  415  -421  1990  [Not refereed][Not invited]
     
    Fundamental evaluation of the subrenal capsule assay (SRCA) method in nonsolid tumors was made, using two types of murine malignant ascites. Malignant ascites were obtained from mice bearing M-5076 ovarian reticular cell sarcoma or MH-134 hepatoma. These tumor cells were allowed to settle by standing at 4℃ to form a jelly-like clot. This clot was cut into fragments about 1mm^3 in size and one of these fragments was mashed in trypan blue to estimate the viability grade of the implanted tumor cells. The rest of the fragments were implanted beneath the renal capsule of the mice. On the 6th day after implantation, the assay mice were killed, the increase in the size of the tumor was determined and histological examination was carried out. The results were as follows : (1) The clot was formed reproductively by allowing ascites to settle for one or two days and there was a high viability rate for the tumor cells: 79.9+11.0% of M-5076 and 90.1+5.9% of MH-134. (2) The ascites clot thus implanted grew rapidly in the control groups but growth was inhibited by chemotherapy : Tumors were reduced significantly (p<0.05-0.005) in the group treated with a single agent. This trend towards a suppressive effect of carcinocidal agents on the tumor growth was more conspicuous as a combination regimen was utilized, a combination of three agents producing the maximum effect. (3) The clot grew more quickly than the solid tumor in both the control and the treated groups. There was a high correlation (r=0.93 in M-5076, and r=0.64 in MH-134) between the growth rates of ascites and solid tumor in S RCA. (4) Histological examination revealed that viable tumor cells infiltrated widely under the renal capsule in both types of tumors. These results suggest that ascites and solid tumor are useful materials for the subrenal capsule assay method.


Copyright © MEDIA FUSION Co.,Ltd. All rights reserved.