A5046992137- PI3K/AKT/mTOR signaling in cancer
- Biochemical and Molecular Research
- Cancer-related gene regulation
- MicroRNA in disease regulation
- RNA Interference and Gene Delivery
- Cancer Mechanisms and Therapy
- Cancer-related molecular mechanisms research
- interferon and immune responses
- RNA Research and Splicing
- Cell death mechanisms and regulation
- Melanoma and MAPK Pathways
- Kruppel-like factors research
- Bioactive natural compounds
- Quinazolinone synthesis and applications
- Pulmonary Hypertension Research and Treatments
- Tea Polyphenols and Effects
- Synthesis of Organic Compounds
- Advanced biosensing and bioanalysis techniques
- Fibroblast Growth Factor Research
- PARP inhibition in cancer therapy
- Signaling Pathways in Disease
- Circular RNAs in diseases
Taiho Pharmaceutical (Japan)
2019-2023
Tokushima University
2019
Gifu University
2012-2013
MicroRNAs regulate gene expression by repressing translation or directing sequence-specific degradation of their complementary mRNA. We recently reported that miR-203 is down-regulated, and its exogenous inhibits cell growth in canine oral malignant melanoma tissue specimens as well human cells. A microRNA target database predicted E2F3 ZBP-89 putative targets microRNA-203 (miR-203). The levels E2F3a, E2F3b, were markedly up-regulated Mewo cells compared with those epidermal melanocytes....
We recently reported that microRNA (miR)-145 is downregulated and induces apoptosis in human bladder cancer cells. Also, it suggested the ectopic expression of miR-145 with induction TRAIL several Here, we demonstrated a novel mechanism by Exogenous T24 NKB1 cells markedly increased levels interferon (IFN)-β, 2′–5′-oligoadenylate synthetase 1, which lies upstream 2′–5′ oligoadenylates/RNase L system, TRAIL, induced apparent caspase-dependent was suppressed cotreatment pan-caspase inhibitor;...
microRNA (miR)-205 is downregulated and acts as a tumor suppressor in human melanoma cells. Previously, for clinical application, we added aromatic benzene-pyridine (BP-type) analogs to the 3′-overhang region of RNA-strand changed sequences passenger strand miR-143 duplex. Here, demonstrated antitumor effect vitro vivo miR-205 that was also chemically modified by BP had altered sequence. In experiments, transfection with synthetic (miR-205BP/S3) significantly inhibited growth Exogenous...
Trabectedin is a DNA-damaging agent and has been approved for the treatment of patients with advanced soft tissue sarcoma. Schlafen 11 (SLFN11) was identified as dominant determinant response to agents. The aim study clarify association between SLFN11 expression antitumor activity trabectedin.The trabectedin evaluated under different levels regulated by RNA interference CRISPR-Cas9 systems, combined ataxia telangiectasia Rad3-related protein kinase (ATR) inhibitor in sarcoma cell lines using...
Abstract The MAPK and PI3K pathways are involved in cancer growth survival; however, the clinical efficacy of single inhibitors each pathway is limited or transient owing to resistance mechanisms, such as feedback signaling and/or reexpression receptor-type tyrosine kinases (RTK). This study identified a potent novel kinase inhibitor, TAS0612, characterized its properties. We found that TAS0612 potent, orally available compound can inhibit p90RSK (RSK), AKT, p70S6K (S6K) agent showed strong...
<p>Supplementary Figure 2. Pharmacodynamic marker inhibitions in the HCC70 tumor xenografts treated after repetitive doses of TAS0612. TAS0612, 60 mg/kg, was administered to tumor-bearing mice daily from Day 1 8 by oral gavage, and subcutaneously implanted tumors were dissected at 4 hour post-administration on 8. After sampling, immunoblot analysis performed detect pharmacodynamic inhibitions, signal feedback, apoptosis induction. Clear inhibition markers such as phospho-PRAS40,...
<p>Supplementary Figure 2. Pharmacodynamic marker inhibitions in the HCC70 tumor xenografts treated after repetitive doses of TAS0612. TAS0612, 60 mg/kg, was administered to tumor-bearing mice daily from Day 1 8 by oral gavage, and subcutaneously implanted tumors were dissected at 4 hour post-administration on 8. After sampling, immunoblot analysis performed detect pharmacodynamic inhibitions, signal feedback, apoptosis induction. Clear inhibition markers such as phospho-PRAS40,...
<p>Supplementary Figure 1. Body weight change of each treatment group corresponding to efficacy study shown in Fig. 6B-6E are panel A-D, respectively. In all studies, there was no evidence intolerance, such as rapid and severe reduction. The on Day 0 defined 100%, the increase or decrease measurement day relative is a percentage (mean ± standard error).</p>
<div>Abstract<p>The MAPK and PI3K pathways are involved in cancer growth survival; however, the clinical efficacy of single inhibitors each pathway is limited or transient owing to resistance mechanisms, such as feedback signaling and/or reexpression receptor-type tyrosine kinases (RTK). This study identified a potent novel kinase inhibitor, TAS0612, characterized its properties. We found that TAS0612 potent, orally available compound can inhibit p90RSK (RSK), AKT, p70S6K (S6K)...
<p>Supplementary Figure 1. Body weight change of each treatment group corresponding to efficacy study shown in Fig. 6B-6E are panel A-D, respectively. In all studies, there was no evidence intolerance, such as rapid and severe reduction. The on Day 0 defined 100%, the increase or decrease measurement day relative is a percentage (mean ± standard error).</p>
<div>Abstract<p>The MAPK and PI3K pathways are involved in cancer growth survival; however, the clinical efficacy of single inhibitors each pathway is limited or transient owing to resistance mechanisms, such as feedback signaling and/or reexpression receptor-type tyrosine kinases (RTK). This study identified a potent novel kinase inhibitor, TAS0612, characterized its properties. We found that TAS0612 potent, orally available compound can inhibit p90RSK (RSK), AKT, p70S6K (S6K)...
Abstract Background: TAS-117 is a potent oral allosteric non-ATP inhibitor selective for AKT. A phase 1 study with ongoing in patients endometrial cancer and ovarian clear cell carcinoma. Futibatinib (TAS-120) selective, irreversible small-molecule fibroblast growth factor receptor (FGFR) 1-4 inhibitor, antiproliferative activity preclinical models FGFR aberrations. Phase 2 studies are various FGFR-deregulated cancers. We evaluated the antitumor of futibatinib plus FGFR-aberrant models....