Dong Xiao1, Xiangyan Cui1, Ning Fang1, Shujian Yu1, Xin Wang1. 1. Department of Otolaryngology-Head and Neck Surgery, The First Hospital of Jilin University Changchun 130021, People's Republic of China.
Abstract
BACKGROUND: It is reported that long non-coding RNA is crucial in many cancer progressions. But the function and regulatory mechanism of LINC01303 in human laryngeal squamous cell carcinoma (LSCC) remains unclear. Hence, this research aims at investigating the biological function and potential mechanism of LINC01303 in LSCC. METHODS: Real-time quantitative PCR (qRT-PCR) was applied for the determination of LINC01303, miR-200c and TIMP metallopeptidase inhibitor 2 (TIMP2) expression in LSCC tissues and cell lines. Corresponding experiments were carried out to determine the impacts of LINC01303 on LSCC cell proliferation, apoptosis, migration and invasion. The interaction between LINC01303 and miR-200c was analyzed with bioinformatics analysis and luciferase activity analysis. RESULTS: LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues. High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration. Mechanically, LINC01303 acted as carcinogenic lncRNA in LSCC by regulating miR-200c/TIMP2 axis. CONCLUSION: LINC01303 plays a carcinogenic part in LSCC carcinogenesis through regulating miR-200c/TIMP2 axis, which may become a promising target of LSCC therapy. AJTR
BACKGROUND: It is reported that long non-coding RNA is crucial in many cancer progressions. But the function and regulatory mechanism of LINC01303 in human laryngeal squamous cell carcinoma (LSCC) remains unclear. Hence, this research aims at investigating the biological function and potential mechanism of LINC01303 in LSCC. METHODS: Real-time quantitative PCR (qRT-PCR) was applied for the determination of LINC01303, miR-200c and TIMP metallopeptidase inhibitor 2 (TIMP2) expression in LSCC tissues and cell lines. Corresponding experiments were carried out to determine the impacts of LINC01303 on LSCC cell proliferation, apoptosis, migration and invasion. The interaction between LINC01303 and miR-200c was analyzed with bioinformatics analysis and luciferase activity analysis. RESULTS:LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues. High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration. Mechanically, LINC01303 acted as carcinogenic lncRNA in LSCC by regulating miR-200c/TIMP2 axis. CONCLUSION:LINC01303 plays a carcinogenic part in LSCC carcinogenesis through regulating miR-200c/TIMP2 axis, which may become a promising target of LSCC therapy. AJTR
Authors: Tomas Tokar; Chiara Pastrello; Andrea E M Rossos; Mark Abovsky; Anne-Christin Hauschild; Mike Tsay; Richard Lu; Igor Jurisica Journal: Nucleic Acids Res Date: 2018-01-04 Impact factor: 16.971