Takuya Shirakihara

ORCID: 0000-0002-6222-0143
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About
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Research Areas
  • TGF-β signaling in diseases
  • Cancer Cells and Metastasis
  • Fibroblast Growth Factor Research
  • Cancer-related gene regulation
  • Epigenetics and DNA Methylation
  • Cancer Mechanisms and Therapy
  • Cancer-related molecular mechanisms research
  • Cancer Genomics and Diagnostics
  • Circular RNAs in diseases
  • Parathyroid Disorders and Treatments
  • Connective Tissue Growth Factor Research
  • Chromatin Remodeling and Cancer
  • Cell death mechanisms and regulation
  • Metastasis and carcinoma case studies
  • Genomics and Phylogenetic Studies
  • Wnt/β-catenin signaling in development and cancer
  • Ubiquitin and proteasome pathways
  • Cell Adhesion Molecules Research
  • Kruppel-like factors research
  • Genetic factors in colorectal cancer
  • interferon and immune responses
  • Pancreatic and Hepatic Oncology Research
  • Hedgehog Signaling Pathway Studies
  • Melanoma and MAPK Pathways
  • Cancer, Hypoxia, and Metabolism

Juntendo University
2024

Kitasato University
2017-2022

National Cancer Centre Japan
2015

The University of Tokyo
2004-2013

National Cancer Research Institute
2011

Japanese Foundation For Cancer Research
2008

Epithelial-mesenchymal transition (EMT), a crucial event in cancer progression and embryonic development, is induced by transforming growth factor (TGF)-beta mouse mammary NMuMG epithelial cells. Id proteins have previously been reported to inhibit major features of TGF-beta-induced EMT. In this study, we show that expression the deltaEF1 family proteins, (ZEB1) SIP1, gradually increased TGF-beta with profiles reciprocal E-cadherin. SIP1 each dramatically down-regulated transcription...

10.1091/mbc.e07-03-0249 article EN Molecular Biology of the Cell 2007-07-06

The epithelial-mesenchymal transition (EMT) is a crucial morphological event that occurs during the progression of epithelial tumors. EMT can be induced by transforming growth factor (TGF)-beta in some tumor cells. Here, we demonstrate molecular mechanism whereby Snail, key regulator EMT, TGF-beta Snail induction was highly dependent on cooperation with active Ras signals, and silencing abolished pancreatic cancer Panc-1 Transfection constitutively into HeLa cells led to TGF-beta, while...

10.1074/jbc.m804777200 article EN cc-by Journal of Biological Chemistry 2008-11-15

Genetic alterations and deregulation of the miRNA biogenesis pathway components have been reported in human tumors. Tissue-specific deletion Dicer gene, which encodes an essential processing enzyme, promotes carcinogenesis animal models. These features indicate that aberrant are directly associated with cancer. For present study, we conducted quantitative RT-PCR 14 genes related to 47 paired samples primary hepatocellular carcinoma (HCC) matched non-cancerous liver. Expression seven (Dgcr8,...

10.1111/cas.12126 article EN Cancer Science 2013-02-09

Epithelial-mesenchymal transition (EMT) is a crucial event in wound healing, tissue repair, and cancer progression adult tissues. Transforming growth factor (TGF)-β induces EMT mouse epithelial cells. During prolonged treatment, TGF-β successively myofibroblastic differentiation with increased expression of myofibroblast marker proteins, including smooth muscle α actin calponin. We recently showed that fibroblast factor-2 prevented induced by TGF-β, transdifferentiated the cells to those...

10.1111/cas.12220 article EN other-oa Cancer Science 2013-06-20

Bone morphogenetic proteins (BMPs) regulate various biological processes, mostly mediated by cells of mesenchymal origin. However, the roles BMPs in epithelial are poorly understood. Here, we demonstrate that, polarized cells, BMP signals transmitted from receptor complexes exclusively localized at basolateral surface cell membrane. In addition, stimulation with increased expression components tight junctions and enhanced transepithelial resistance (TER), counteracting reduction TER...

10.1371/journal.pone.0062659 article EN cc-by PLoS ONE 2013-05-13

10.1016/j.bbrc.2009.02.098 article EN Biochemical and Biophysical Research Communications 2009-02-25

The epithelial-mesenchymal transition (EMT) is associated with tumor progression. We reported previously that expression of the δEF1 family proteins (δEF1/ZEB1 and SIP1/ZEB2), key regulators EMT, positively correlated EMT phenotypes aggressiveness breast cancer. Here, we show levels regulator G-protein signaling 16 (RGS16) are negatively those proteins. On basis results gain- loss-of-function analyses, suggest promote cell motility cancer cells directly or indirectly through repressing RGS16.

10.1002/1873-3468.12042 article EN cc-by-nc-nd FEBS Letters 2015-12-21

Abstract Epithelial mesenchymal transition (EMT) is a crucial event in appropriate embryonic development as well wound healing, tissue repair, and cancer progression adult tissues. EMT endows cells with migratory invasive properties, inhibits apoptosis senescence, contributes to immunosuppression, induces stress resistance stem cell properties. We have recently demonstrated that transforming growth factor (TGF)-β isoform switching of fibroblast (FGF) receptors through regulating expression...

10.1158/1538-7445.tim2013-a76 article EN Cancer Research 2013-02-01

Diffuse-type gastric carcinoma (DGC) is highly invasive subtype of adenocarcinomas and frequently exhibit scattered peritoneal metastasis. Previous studies have shown that genes receptor tyrosine kinases (RTKs) such as FGFR2 or Met are amplified in DGC cell lines with high frequency. Hence, these cells oncogene addiction to sustained activity RTKs for maintenance malignant phenotype. In order gain novel insight the downstream signaling pathway DGC-specific RTKs, phosphoproteomic analysis was...

10.1158/1538-7445.sabcs18-857 article EN Molecular and Cellular Biology / Genetics 2019-07-01

Abstract Diffuse-type gastric carcinoma (DGC) is highly invasive subtype of adenocarcinomas and frequently exhibit scattered peritoneal metastasis. Previous studies have shown that genes receptor tyrosine kinases (RTKs) such as FGFR2 or Met are amplified in DGC cell lines with high frequency. Hence, these cells oncogene addiction to sustained activity RTKs for maintenance malignant phenotype. In order gain novel insight the downstream signaling pathway DGC-specific RTKs, phosphoproteomic...

10.1158/1538-7445.am2019-857 article EN Cancer Research 2019-07-01
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