- RNA Research and Splicing
- Metabolism, Diabetes, and Cancer
- Cancer-related gene regulation
- Lipid metabolism and biosynthesis
- Adipose Tissue and Metabolism
- Inflammatory mediators and NSAID effects
- Nuclear Structure and Function
- PI3K/AKT/mTOR signaling in cancer
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- Pancreatic function and diabetes
- Immune cells in cancer
- Cell death mechanisms and regulation
- Chemokine receptors and signaling
- 14-3-3 protein interactions
Okayama University
2022-2024
Okinawa Institute of Science and Technology Graduate University
2015
Uncoupling protein 1 (Ucp1) contributes to thermogenesis, and its expression is regulated at the transcriptional level. Here, we show that Ucp1 also post-transcriptionally. In inguinal white adipose tissue (iWAT) of mice fed a high-fat diet (HFD), level decreases concomitantly with increases in Cnot7 interacting partner Tob. HFD-fed lacking Tob express elevated levels mRNA iWAT are resistant diet-induced obesity. has an elongated poly(A) tail persists Cnot7(-/-) and/or Tob(-/-) on HFD....
Abstract NF-κB mediates transcriptional regulation crucial to many biological functions, and elevated activity leads autoimmune inflammatory diseases, as well cancer. Since highly aggressive breast cancers have few therapeutic molecular targets, clarification of key mechanisms signaling would facilitate the development more effective therapy. In this report, we show that Tob, a member Tob/BTG family antiproliferative proteins, acts negative regulator signal in Studies with 35 human cancer...
Abstract The CCR4-NOT complex is conserved in eukaryotes and involved mRNA metabolism, though its molecular physiological roles remain to be established. We show here that CNOT3-depleted mouse embryonic fibroblasts (MEFs) undergo cell death. Levels of other subunits are decreased MEFs. death phenotype rescued by introduction wild-type (WT), but not mutated CNOT3 suppressed the pan-caspase inhibitor, zVAD-fluoromethylketone. Gene expression profiling reveals mRNAs encoding death-related...
Metformin (Met), a first-line drug for type 2 diabetes, lowers blood glucose levels by suppressing gluconeogenesis in the liver, presumably through liver kinase B1-dependent activation of AMP-activated protein (AMPK) after inhibiting respiratory chain complex I. Met is also implicated as to be repurposed cancers; its mechanism believed identical that inhibition. However, AMPK requires high concentrations at more than 1 mM, which are unachievable vivo . The immune-mediated antitumor response...
Tumor blood vessels are highly leaky in structure and have poor perfusion, which hampers infiltration function of CD8T cells within tumor. Normalizing tumor is thus thought to be important promoting the flux immune T enhancing ant-tumor immunity. However, how vasculature normalized poorly understood. Metformin (Met) combined with ant-PD-1 therapy known stimulate proliferation produce large amounts IFNγ from tumor-infiltrating lymphocytes (CD8TILs). We found that combination promotes pericyte...
Abstract Prostaglandin E2 (PGE2), a product of the cyclooxygenase (COX) pathway, is produced by tumors and surrounding stromal cells. It stimulates tumor progression, promotes angiogenesis suppresses anti-tumor response. Pharmacological inhibition PGE2 synthesis has been shown to suppress initiation growth in vivo. In current study, we demonstrated that Ptgs2-deficient 3LL lung adenocarcinoma cell line was down-regulated vivo through natural killer (NK) activation reduction population...
Abstract NF-κB mediates transcriptional regulation crucial to many biological functions, and elevated activity leads autoimmune inflammatory diseases, as well cancer. Since highly aggressive breast cancers have few therapeutic molecular targets, clarification of key mechanisms signaling would facilitate development more effective therapy. In this report, we show that Tob, a member the Tob/BTG family antiproliferative proteins, acts negative regulator signal in Studies with 35 human cancer...