miR-135b reverses chemoresistance of non-small cell lung cancer cells by downregulation of FZD1 |
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| Institution: | 1. Department of Oncology, Affiliated Hospital of Guangdong Medical College, 57 Renmin Road, Zhanjiang, PR China;2. The Tumor Hospital of Chengdu, Department of Radiotherapy, The Seventh People’s Hospital of Chengdu, Chengdu 610041, Sichuan, PR China;3. Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical College, 57 Renmin Road, Zhanjiang, PR China;4. Department of Histology and Embryology, Guangdong Medical College, Dongguan 523808, Guangdong, PR China;5. Department of Oncology, Zhanjinag Central People’s Hospital, 2 Cunjin Road, Zhanjiang, Guangdong, PR China;1. School of Medical and Molecular Biosciences at the University of Technology Sydney (UTS), 15 Broadway, Ultimo, NSW 2007, Australia;2. School of Software, Faculty of Engineering and Information Technology and the Centre for Quantum Computation and Intelligent Systems at the University of Technology Sydney (UTS), 15 Broadway, Ultimo, NSW 2007, Australia;1. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, James Buchanan Brady Urological Institute and Department of Urology, Johns Hopkins School of Medicine and Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland;2. Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland;3. Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland;4. Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland;5. SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, Washington;6. Cancer Prevention Program, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington;7. Center for Clinical and Translational Research, Cleveland Clinic Lerner College of Medicine, Cleveland, Ohio;8. University of Colorado Denver School of Medicine, Aurora, Colorado;9. Department of Urology, University of Texas Health Sciences Center San Antonio, San Antonio, Texas;1. Department of Urology, University of Texas M.D. Anderson Cancer Center, Houston, Texas;2. Department of Biostatistics, University of Texas M.D. Anderson Cancer Center, Houston, Texas;3. Department of Pathology, University of Texas M.D. Anderson Cancer Center, Houston, Texas;4. Department of Genitourinary Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas;1. Department of General Surgery, Section of Plastic Reconstructive and Aesthetic Surgery, Tan Tock Seng Hospital, Singapore;2. Department of General Surgery, Singapore General Hospital, Singapore;1. College of Mathematics and Information Technology, Hebei Normal University of Science and Technology, Qinhuangdao 066004, PR China;2. College of Marine Life Science, Ocean University of China, Yushan Road, Qingdao 266003, PR China |
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| Abstract: | BackgroundNon-small cell lung cancer (NSCLC) chemoresistance usually limits the clinical efficacy of chemotherapeutic approaches. However, few reports have revealed the regulation of miR-135b and Frizzled-1 (FZD1) involved in NSCLC chemoresistance.MethodsTo identify the mechanism of miR-135b and FZD1 in NSCLC chemoresistance and to observe their biological functions, we detected the expression levels of miR-135b and FZD1 by conducting quantitative real-time polymerase chain reaction (RT-qPCR) and modified the expressions of miR-135b and FZD1 by transiently transfecting cells with miR-135b mimics or FZD1-siRNA. The 3′-untranslated region (3′-UTR) of FZD1 combined with miR-135b was verified through dual-luciferase reporter assay.ResultsCompared with that in A549 parental cell lines, the miR-135b expression in drug-resistant lung cancer cell lines (A549/DDP) was decreased and their FZD1 expression was increased. The increased miR-135b expression and silenced FZD1 expression enhanced the sensitivity of resistant cells to cisplatin treatment. The high expression of miR-135b in A549/DDP cells remarkably decreased the mRNA levels of FZD1. FZD1 was further identified as the functional downstream target of miR-135b by directly targeting the 3′-UTR of FZD1.ConclusionThe amplification of miR-135b suppressed NSCLC chemoresistance by directly mediating the FZD1 downregulation. |
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| Keywords: | miR-135b FZD1 Chemoresistance NSCLC |
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