LINC01354 enhances the proliferation and invasion of lung cancer cells by regulating miR-340-5p/ATF1 signaling pathway
Autor: | Zuojun Shen, Gaojie Yang, Chongyi Yang, Peng Gao, Yahui She |
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Rok vydání: | 2019 |
Předmět: |
Lung Neoplasms
Biomedical Engineering Pharmaceutical Science Medicine (miscellaneous) 02 engineering and technology Biology 03 medical and health sciences 0302 clinical medicine Competitive binding Carcinoma Non-Small-Cell Lung Cell Line Tumor medicine Humans Neoplasm Invasiveness Lung cancer Cell Proliferation Gene knockdown Base Sequence ATF1 Mechanism (biology) Proteins General Medicine 021001 nanoscience & nanotechnology medicine.disease In vitro Up-Regulation respiratory tract diseases MicroRNAs Cell culture Gene Knockdown Techniques 030220 oncology & carcinogenesis Disease Progression Cancer research RNA Long Noncoding Signal transduction 0210 nano-technology Signal Transduction Biotechnology |
Zdroj: | Artificial Cells, Nanomedicine, and Biotechnology. 47:3737-3744 |
ISSN: | 2169-141X 2169-1401 |
DOI: | 10.1080/21691401.2019.1667816 |
Popis: | Recent studies showed that long non-coding RNAs (lncRNAs) could play critical roles in tumors progression. However, the performance of LINC01354 is still limited in non-small cell lung cancer (NSCLC). In the current study, our results showed that LINC01354 was significantly increased in NSCLC tissues and cell lines. High LINC01354 expression was associated with advanced TNM stage and poor prognosis in NSCLC patients. Loss-of-function assays revealed that knockdown of LINC01354 reduced lung cancer cells proliferation and invasive ability in vitro. Subsequently, mechanism studies showed that LINC01354 positively regulated the ATF1 expression via competitive binding to miR-340-5p. Therefore, our results illustrated that LINC01354 might act as an oncogenic role by modulating the miR-340-5p/ATF1 axis, providing a novel therapeutic therapy for NSCLC treatment. |
Databáze: | OpenAIRE |
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