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Your search keyword '"Ruiying Sun"' showing total 2 results
Start Over Author "Ruiying Sun" Journal bioscience reports
2 results on '"Ruiying Sun"'

1. lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressor miR-615-5p

Author

Miaoyi Huang, Yu Dong, Ruiying Sun, Zhiyan Liu, Shuanying Yang, and Xiaoying Huo

Subjects
0301 basic medicine, A549 cell, Gene knockdown, Chemistry, Cell growth, Biophysics, AKT2, Cell Biology, Transfection, medicine.disease, Biochemistry, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Apoptosis, Cell culture, 030220 oncology & carcinogenesis, Cancer research, medicine, Lung cancer, Molecular Biology
Abstract

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P

Published
2018

2. lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressor

Author

Yu, Dong, Xiaoying, Huo, Ruiying, Sun, Zhiyan, Liu, Miaoyi, Huang, and Shuanying, Yang

Subjects
Adult, Male, Lung Neoplasms, Apoptosis, cell proliferation and invasion, Insulin-Like Growth Factor II, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Humans, Neoplasm Invasiveness, RNA, Small Interfering, Research Articles, non-small cell lung cancer, Cell Proliferation, Glycine Hydroxymethyltransferase, RNA interaction, Oligoribonucleotides, Base Sequence, Antagomirs, Middle Aged, respiratory tract diseases, Gene Expression Regulation, Neoplastic, MicroRNAs, miR-615-5p, Female, RNA, Long Noncoding, lncRNA Gm15290, Proto-Oncogene Proteins c-akt, Signal Transduction, Research Article
Abstract

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P

Published
2018

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