J-Z Yang1, L Bian, J-G Hou, H-Y Wang. 1. Department of Radiation Oncology, The Second Hospital of Jilin University, Changchun, China. 27382909@qq.com.
Abstract
OBJECTIVE: MicroRNAs (miRNAs) have been identified to play a crucial regulatory role in the development and progression of malignant tumors, including lung cancer. However, the function of miR-550a-3p on the progression of non-small cell lung cancer (NSCLC) remains poorly understood. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction was employed to estimate the expression level of miR-550a-3p in NSCLC tissue and cell samples. Cell proliferation was measured by using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and colony formation assays. Transwell assay was recruited to demonstrate the abilities of cell invasion and migration. Luciferase analysis and Western-blot assay were performed to elucidate the underlying mechanism of miR-550a-3p in NSCLC. RESULTS: The level of miR-550a-3p expressed in NSCLC tissues was significantly higher than that in para-tumor control tissues. Over-expression of miR-550a-3p significantly promoted proliferation, invasion, and migration of A549 cells while knockdown of miR-550a-3p inhibited growth and metastasis of H460 cells. TIMP2 was verified as a direct target of miR-550a-3p in NSCLC. Restoration of TIMP2 rescued the influence of miR-550a-3p over-expression. CONCLUSIONS: We demonstrated that miR-550a-3p regulated the progression of NSCLC cells through TIMP2. Thus, miR-550a-3p axis could serve as a potential therapeutic target for NSCLC treatment.
OBJECTIVE: MicroRNAs (miRNAs) have been identified to play a crucial regulatory role in the development and progression of malignant tumors, including lung cancer. However, the function of miR-550a-3p on the progression of non-small cell lung cancer (NSCLC) remains poorly understood. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction was employed to estimate the expression level of miR-550a-3p in NSCLC tissue and cell samples. Cell proliferation was measured by using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and colony formation assays. Transwell assay was recruited to demonstrate the abilities of cell invasion and migration. Luciferase analysis and Western-blot assay were performed to elucidate the underlying mechanism of miR-550a-3p in NSCLC. RESULTS: The level of miR-550a-3p expressed in NSCLC tissues was significantly higher than that in para-tumor control tissues. Over-expression of miR-550a-3p significantly promoted proliferation, invasion, and migration of A549 cells while knockdown of miR-550a-3p inhibited growth and metastasis of H460 cells. TIMP2 was verified as a direct target of miR-550a-3p in NSCLC. Restoration of TIMP2 rescued the influence of miR-550a-3p over-expression. CONCLUSIONS: We demonstrated that miR-550a-3p regulated the progression of NSCLC cells through TIMP2. Thus, miR-550a-3p axis could serve as a potential therapeutic target for NSCLC treatment.