Tatsuya Kato1, Hironobu Wada2, Priya Patel3, Hsin-Pei Hu3, Daiyoon Lee3, Hideki Ujiie3, Kentaro Hirohashi3, Takahiro Nakajima4, Masaaki Sato5, Mitsuhito Kaji6, Kichizo Kaga7, Yoshiro Matsui7, Ming-Sound Tsao8, Kazuhiro Yasufuku9. 1. Division of Thoracic Surgery, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada; Department of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan. 2. Division of Thoracic Surgery, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada; Department of General Thoracic Surgery, Chiba University Chiba Graduate School of Medicine, Chiba, Japan. 3. Division of Thoracic Surgery, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada. 4. Department of General Thoracic Surgery, Chiba University Chiba Graduate School of Medicine, Chiba, Japan. 5. Department of Pathology, NTT East Japan Sapporo Hospital, Sapporo 060-0061, Japan. 6. Department of Thoracic Surgery, Sapporo Minami-sanjo Hospital, Sapporo, Hokkaido, Japan. 7. Department of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan. 8. Departments of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Department of Pathology, University Health Network, Toronto, Ontario, Canada. 9. Division of Thoracic Surgery, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada. Electronic address: kazuhiro.yasufuku@uhn.ca.
Abstract
OBJECTIVE: High-level expression of kinesin family member 23 (KIF23), a member of microtubule-dependent molecular motors that transport organelles within cells and move chromosomes during cell division, has been observed in a variety of human malignancies. The aims of the present study were to observe the expression of KIF23 in lung cancer, examine the role of KIF23 in lung cancer cell growth and/or survival by small interfering RNA experiments, and explore its clinicopathologic significance and evaluate KIF23 expression as a prognostic marker. MATERIALS AND METHODS: Quantitative reverse transcription-polymerase chain reaction analysis was performed to detect the expression of KIF23 mRNA using metastatic lymph nodes from patients with advanced lung cancer obtained by endobronchial ultrasonography-guided transbronchial needle aspiration (EBUS-TBNA) and primary lung tumors through surgical sample. The role of KIF23 in cancer cell growth was examined by small interfering RNA experiments. A total of 339 lung cancers were analyzed immunohistochemically on tissue microarrays to examine the expression of KIF23 protein and its clinicopathologic significance. RESULTS: KIF23 transcript was found to be overexpressed in the great majority of metastatic lymph nodes from advanced lung cancers and primary lung tumors. Inhibiting KIF23 expression effectively suppressed lung cancer cell growth. High-level KIF23 expression was observed in 67.8% of the 339 cases. Lung adenocarcinoma patients with tumors displaying a high-level of KIF23 expression was also identified as an independent prognostic factor by multivariate analysis (P=0.0064). CONCLUSION: KIF23 not only provides additional prognostic information for surgical treatment of lung cancer, but may also be a novel therapeutic target for these patients.
OBJECTIVE: High-level expression of kinesin family member 23 (KIF23), a member of microtubule-dependent molecular motors that transport organelles within cells and move chromosomes during cell division, has been observed in a variety of humanmalignancies. The aims of the present study were to observe the expression of KIF23 in lung cancer, examine the role of KIF23 in lung cancer cell growth and/or survival by small interfering RNA experiments, and explore its clinicopathologic significance and evaluate KIF23 expression as a prognostic marker. MATERIALS AND METHODS: Quantitative reverse transcription-polymerase chain reaction analysis was performed to detect the expression of KIF23 mRNA using metastatic lymph nodes from patients with advanced lung cancer obtained by endobronchial ultrasonography-guided transbronchial needle aspiration (EBUS-TBNA) and primary lung tumors through surgical sample. The role of KIF23 in cancer cell growth was examined by small interfering RNA experiments. A total of 339 lung cancers were analyzed immunohistochemically on tissue microarrays to examine the expression of KIF23 protein and its clinicopathologic significance. RESULTS:KIF23 transcript was found to be overexpressed in the great majority of metastatic lymph nodes from advanced lung cancers and primary lung tumors. Inhibiting KIF23 expression effectively suppressed lung cancer cell growth. High-level KIF23 expression was observed in 67.8% of the 339 cases. Lung adenocarcinomapatients with tumors displaying a high-level of KIF23 expression was also identified as an independent prognostic factor by multivariate analysis (P=0.0064). CONCLUSION:KIF23 not only provides additional prognostic information for surgical treatment of lung cancer, but may also be a novel therapeutic target for these patients.
Authors: Samantha Weed; Blair Armistead; Michelle Coleman; H Denny Liggit; Brian Johnson; Jesse Tsai; Richard P Beyer; Theodor K Bammler; Nicole M Kretzer; Ed Parker; Jeroen P Vanderhoeven; Craig J Bierle; Lakshmi Rajagopal; Kristina M Adams Waldorf Journal: J Infect Dis Date: 2020-10-13 Impact factor: 5.226