Ching-Chih Lee1, Hsu-Chueh Ho1, Yu-Chieh Su2, Moon-Sing Lee3, Shih-Kai Hung3, Chun-Hsuan Lin4. 1. Department of Otolaryngology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. 2. School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. Division of Hematology-Oncology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. 3. School of Medicine, Tzu Chi University, Hualian, Taiwan, R.O.C. Department of Radiation Oncology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. 4. Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. kumar1119@yahoo.com.tw.
Abstract
AIM: To explore whether monocyte chemotactic protein-1 (MCP1) is associated with the epithelial-mesenchymal transition (EMT) and neck metastases in head and neck cancer (HNC). MATERIALS AND METHODS: MCP1 and its related protein were evaluated using western blotting, and a migration assay for HNC cell lines. Thirty-five patients with HNC were recruited for the evaluation of MCP1 expression and pathologically-proven neck metastases from their tissue specimens. RESULTS: MCP1 changed the phenotype of OML-1 cells to a spindle shape, with increased mobility. In OML3 cells, MCP1 knockdown with siRNA blocked EMT. Activation of protein kinase B (AKT) was positively associated with the EMT phenotype, and this transition was abrogated with a phosphoinositide 3 kinase (PI3K) inhibitor. By comparing clinical outcomes, the histological MCP1 score was associated with pathological neck metastases (p=0.027). CONCLUSION: The overexpression of MCP1 in HNC cells may partially induce EMT through the AKT pathway. A high cellular expression of MCP1 was associated with pathological neck metastases. Copyright
AIM: To explore whether monocyte chemotactic protein-1 (MCP1) is associated with the epithelial-mesenchymal transition (EMT) and neck metastases in head and neck cancer (HNC). MATERIALS AND METHODS:MCP1 and its related protein were evaluated using western blotting, and a migration assay for HNC cell lines. Thirty-five patients with HNC were recruited for the evaluation of MCP1 expression and pathologically-proven neck metastases from their tissue specimens. RESULTS:MCP1 changed the phenotype of OML-1 cells to a spindle shape, with increased mobility. In OML3 cells, MCP1 knockdown with siRNA blocked EMT. Activation of protein kinase B (AKT) was positively associated with the EMT phenotype, and this transition was abrogated with a phosphoinositide 3 kinase (PI3K) inhibitor. By comparing clinical outcomes, the histological MCP1 score was associated with pathological neck metastases (p=0.027). CONCLUSION: The overexpression of MCP1 in HNC cells may partially induce EMT through the AKT pathway. A high cellular expression of MCP1 was associated with pathological neck metastases. Copyright
Authors: Marketa Svobodova; Martina Raudenska; Jaromir Gumulec; Jan Balvan; Michaela Fojtu; Monika Kratochvilova; Hana Polanska; Zuzana Horakova; Rom Kostrica; Petr Babula; Zbynek Heger; Michal Masarik Journal: Oncotarget Date: 2017-08-03