PDK1 is a potential therapeutic target against angiosarcoma cells

• Published in: Journal of dermatological science Vol. 78; no. 1; pp. 44 - 50
• Main Authors: Wada, Makoto, Horinaka, Mano, Yasuda, Shusuke, Masuzawa, Mikio, Sakai, Toshiyuki, Katoh, Norito
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ireland Ltd 01.04.2015
• Subjects: 3-Phosphoinositide-Dependent Protein Kinases - genetics; 3-Phosphoinositide-Dependent Protein Kinases - metabolism; AKT-independent; Antineoplastic Agents - pharmacology; Apoptosis - drug effects; Cell Line, Tumor; Cell Proliferation - drug effects; Cyclin D; Cyclin D - metabolism; Dermatology; Dose-Response Relationship, Drug; G1 Phase Cell Cycle Checkpoints - drug effects; Hemangiosarcoma - drug therapy; Hemangiosarcoma - enzymology; Hemangiosarcoma - genetics; Hemangiosarcoma - pathology; Humans; Molecular Targeted Therapy; PDK1; Phosphatidylinositol 3-Kinase - antagonists & inhibitors; Phosphatidylinositol 3-Kinase - metabolism; Protein Kinase Inhibitors - pharmacology; Proto-Oncogene Proteins c-akt - antagonists & inhibitors; Proto-Oncogene Proteins c-akt - metabolism; RNA Interference; Signal Transduction - drug effects; Skin Neoplasms - drug therapy; Skin Neoplasms - enzymology; Skin Neoplasms - genetics; Skin Neoplasms - pathology; TOR Serine-Threonine Kinases - antagonists & inhibitors; TOR Serine-Threonine Kinases - metabolism; Transfection; AKT-independent; Cyclin D; PDK1
• ISSN: 0923-1811; 1873-569X
• DOI: 10.1016/j.jdermsci.2015.01.015

Highlights • The PI3K inhibitor and mTOR inhibitor induced G1 cell cycle arrest. • Cyclin D levels were decreased by knockdown of PDK1, not by AKT inhibitor. • The knockdown of PDK1 inhibited colony formation than the mTOR inhibitor.