Gli promotes epithelial-mesenchymal transition in human lung adenocarcinomas

• DOI: 10.18632/oncotarget.11246
• Publication Date: 2016-08-12T20:39:03Z
• Authors: Hui Li; Dongsheng Yue; Joy Q. Jin; Gavitt A. Woodard; Bhairavi Tolani; Thomas M. Luh; Etienne Giroux-Le...; Minli Mo; Zhao Chen; Juanjuan Che; Zhenfa Zhang; Yong Zhou; Lei Wang; Xishan Hao; David Jablons; Changli Wang; Biao He
• Keywords: Male; 0301 basic medicine; Time Factors; Lung Neoplasms; Nude; Mice; Cell Movement; 2.1 Biological and endogenous factors; Aetiology; Lung; gli; Cancer; Lung Cancer; Middle Aged; Cadherins; Smoothened Receptor; CD; Tumor Burden; 3. Good health; Gene Expression Regulation, Neoplastic; 5.1 Pharmaceuticals; Female; Development of treatments and therapeutic interventions; Biotechnology; Research Paper; Signal Transduction; Epithelial-Mesenchymal Transition; Oncology and Carcinogenesis; epithelial-mesenchymal transition; 610; Mice, Nude; Adenocarcinoma of Lung; Antineoplastic Agents; Adenocarcinoma; Zinc Finger Protein GLI1; 576; sonic hedgehog; 03 medical and health sciences; Rare Diseases; Antigens, CD; Animals; Humans; Hedgehog Proteins; Neoplasm Invasiveness; Antigens; Neoplastic; adenocarcinoma; Xenograft Model Antitumor Assays; lung cancer; Orphan Drug; Gene Expression Regulation; A549 Cells

// Hui Li 1, * , Dongsheng Yue 2, Joy Q. Jin 1 Gavitt A. Woodard Bhairavi Tolani Thomas M. Luh Etienne Giroux-Leprieur Minli Mo 3 Zhao Chen Juanjuan Che 4 Zhenfa Zhang 2 Yong Zhou Lei Wang 5 Xishan Hao David Jablons Changli Biao He Thoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University California, San Francisco, CA 94115, USA Lung Cancer, Tianjin Medical Institute and Hospital, 300060, China Beijing ACCB Biotech Ltd., 100084, Oncology, Friendship Hospital Capital University, 100050, Fourth Hebei Shijiazhuang, 050011, These authors have contributed equally to this work Correspondence to: He, email: [e-mail] Wang, [e-mail] Keywords: sonic hedgehog, gli, epithelial-mesenchymal transition, lung cancer, adenocarcinoma Received: May 09, 2016 Accepted: July 28, Published: August 12, ABSTRACT Adenocarcinoma is the most common type cancer. Epithelial-mesenchymal transition (EMT) required for tumor invasion/metastasis components that control process are potential therapeutic targets. This study we examined role Gli in whether its activation regulates metastasis through EMT adenocarcinoma. We found tumors with high expression had significantly lower E-Cadherin two independent cohorts patients studied. In vitro up-regulation SHh resulted increased cell migration while small molecule inhibitors Smo or reduced mobility both a wound healing assay 3D invasion assay. Inhibition vivo decreased growth induced an increase expression. Our results indicate may be critical novel inhibitor shows promise as agent by preventing reducing increasing .