MicroRNA-421 promotes proliferation and invasion of non-small cell lung cancer cells through targeting PDCD4 |
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| Affiliation: | 1. Department of Cardiovascular Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China;2. Department of Thoracic Surgery, Harbin Medical University Cancer Hospital, Harbin, China;3. Department of Pneumoconiosis, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China;1. Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway;2. Faculty of Medicine and Health Sciences, Department of Clinical and Molecular Medicine (IKOM), PO Box 8905, NO-7491 Trondheim, Norway;3. Regional Centre for Child and Youth Mental Health and Child Welfare, Department of Mental Health, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway;4. RKBU Midt-Norge, NTNU, Postboks 8905 MTFS, NO-7491 Trondheim, Norway;5. Department of Pathology, St. Olavs Hospital, Trondheim, Norway;6. St. Olavs hospital HF, Postboks 3250 Torgarden, 7006 Trondheim, Norway;1. Scientific Research Centre, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China;2. Prenatal Diagnosis Center, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China;1. National Atomic Energy Commission, (CNEA), Constituyentes Atomic Center, Research, Applications Management, Av. General, B1650KNA, San Martín, Buenos Aires, Argentina;2. National Scientific and Technical Research Council (CONICET), C1425FQB, CABA, Argentina;3. Italian Hospital of Buenos Aires (HIBA), Department of Dermatology, Experimental Dermatology, C1199ABB, CABA, Argentina;4. Italian Hospital of Buenos Aires (HIBA), Department of Anatomic Pathology, C1199ABB, CABA, Argentina;5. Laboratory of Bioinformatics, Curitiba (PR), Federal University of Paraná (UFPR), Professional and Technological Education Sector, Polytechnic Center Laboratory of Bioinformatics and Systems Biology, PPG-Bioinformática Jardim das Américas, 81531-970, Curitiba, PR, Brazil;6. Federal University of Rio Grande do Sul (UFRGS), Institute of Basic Health Sciences (ICBS), Department of Biochemistry, Laboratory of Cellular Biochemistry, 90035-003, Porto Alegre, RS, Brazil;7. National Institutes of Science & Technology, Translational Medicine (INCT-TM), 90035-903, Porto Alegre, RS, Brazil;8. National University of San Martin, Miguelete Campus, School of Science and Technology, B1650KNA, Villa Lynch, Buenos Aires, Argentina;1. Department of Pathology, Eulji University Hospital, Eulji University School of Medicine, Daejeon, Republic of Korea;2. Department of Internal Medicine, Eulji Hospital, Eulji University School of Medicine, Seoul, Republic of Korea;2. Adelaide Institute for Sleep Health: Flinders Centre of Research Excellence, Flinders University, Bedford Park, South Australia, Australia;3. Respiratory and Sleep Services, Southern Adelaide Local Health Network, Bedford Park, South Australia, Australia;4. Department of Gastroenterology and Hepatology, Flinders Medical Centre, Bedford Park, South Australia, Australia;6. Flinders Centre for Innovation in Cancer, Flinders University, Bedford Park, South Australia, Australia |
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| Abstract: | ![]()
Recent evidence highlights that microRNAs serve as crucial regulators of tumorigenesis, including non-small cell lung cancer (NSCLC). The present study was designed to investigate the expression profile, clinical significance and biological role of miR-421 in NSCLC. The results showed that miR-421 expression was markedly increased in NSCLC tissues and cell lines. Further experimental data indicated that knockdown of miR-421 significantly inhibited NSCLC cell proliferation and induced cell cycle arrest in vitro. The migratory and invasive abilities of NSCLC cells were also attenuated following miR-421 knockdown. Furthermore, PDCD4 was identified as a direct target of miR-421, and its expression was inversely correlated with miR-421 expression in NSCLC tissues. PDCD4 also abrogated the oncogenic role of miR-421 in NSCLC cells. Collectively, our study revealed that miR-421 is significantly upregulated in NSCLC and might represent a potential therapeutic target for NSCLC patients. |
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| Keywords: | Non-small cell lung cancer microRNA-421 PDCD4 Cell cycle Invasion |
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