This is the Department of Applied Pathology, Graduate School of Medicine, The University of Tokyo.
Publications
最近の業績をご紹介します
Inhibition of HVEM suppresses growth and invasion of mesenchymal glioblastoma
Ryo Tanabe, et al
HVEM drives aggressive glioblastoma by boosting tumor growth and invasion upon binding of APRIL, while an anti-HVEM nanobody slows tumor progression.
In vitro functional analysis of lysyl oxidase family members in highly metastatic pancreatic cancer cells derived from a syngeneic orthotopic model
Kei Takahashi-Yamashiro, et al
Serial in vivo selection generated highly metastatic Panc02-3P cells with enhanced tumorigenicity and a mesenchymal-like transcriptional profile. LOX family members (LOX, LOXL1, and LOXL3) were strongly upregulated, and LOX/LOXL1 knockdown suppressed migration. These findings identify LOX family proteins as potential drivers of PDAC metastasis and therapeutic targets.
Downregulation of KRTAP2-3 Suppresses Proliferation and Tumor Formation of Oral Cancer Cells via Inactivation of KRAS Signals
Qianqian Miao, et al
KRTAP2-3 downregulation induced mesenchymal-epithelial transition, reduced proliferation, and suppressed tumor formation in oral squamous cell carcinoma cells. Mechanistically, KRTAP2-3 depletion attenuated KRAS signaling with reduced FGF-5 and FOSL1 expression, and knockdown of either FGF-5 or FOSL1 inhibited cell proliferation. These findings identify KRTAP2-3 as a potential therapeutic target for OSCC.
SMAD1/5-mediated recruitment of the histone demethylase KDM1A controls cell fate programs in embryonic stem cells
Masato Morikawa, et al
BMP signaling via SMAD1/5 plays roles in mESCs, but its function remains unclear. Here, we show that SMAD1/5 recruit KDM1A/LSD1 to specific genomic regions to remove enhancer-associated H3K4me1/2 marks, thereby repressing cell type–specific gene expression. These findings identify a SMAD1/5–KDM1A axis as a key mechanism of transcriptional repression in mESCs.
Receptor-activated transcription factors and beyond: multiple modes of Smad2/3-dependent transmission of TGF-β signaling
Keiji Miyazawa, et al
TGF-β signaling is mediated by receptor-activated Smad proteins, which function as transcription factors downstream of ubiquitously expressed TGF-β family receptors. In addition to transcriptional regulation, Smads control multiple post-transcriptional processes and other signaling pathways, including mitochondrial regulation. This review summarizes these diverse functions and highlights differences between Smad2 and Smad3.
