Jun Zhang1, Xionghuai Hua1, Na Qi2, Guangsen Han3, Juan Yu1, Yongkui Yu4, Xiufeng Wei4, Haomiao Li4, Xiankai Chen4, Changsen Leng4, Qi Liu4, Yingmin Lu5, Yin Li6. 1. Department of Endoscopic Diagnosis and Treatment Center, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Henan, China. 2. Medical Genetic Institute, Henan Provincial People's Hospital, Henan, China. 3. Department of general surgery, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Henan, China. 4. Department of Thoracic Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Henan, China. 5. Department of Thoracic Surgery, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Henan, China. 6. Department of Endoscopic Diagnosis and Treatment Center, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Henan, China. Electronic address: 843901667@qq.com.
Abstract
HEADING AIMS: MicroRNA-27b (miR-27b) has been shown to play a role in the progression of many different forms of cancer, but its specific relevance in the context of non-small cell lung cancer (NSCLC) remains uncertain. As such, this study sought to explore the role of miR-27b in NSCLC and the mechanisms whereby it functions. MATERIALS AND METHODS: We quantified miR-27b and target gene expression via quantitative real-time PCR (RT-qPCR).We then used functional including proliferation assays, migration assay, flow cytometry, and western blotting to explore the mechanisms whereby miR-27b functions in vitro and in vivo. We additionally confirmed miR-27b target genes via luciferase reporter assay. KEY FINDINGS: We observed a marked decrease in miR-27b expression in NSCLC patient samples relative to paracancerous control tissues. We further found that altering miR-27b expression levels in vitro affected NSCLC tumor cell migration, proliferation, and ability to undergo epithelial-mesenchymal transition. Through the use of target prediction algorithms we identified Snail to be a miR-27b target protein that was suppressed when this miRNA was highlight expressed. Lastly, we found miR-27b expression to increase NSCLC cell sensitivity to cisplatin through its ability to target Snail. SIGNIFICANCE: Our results clearly demonstrate that miR-27b can suppress NSCLC tumor development and progression, highlighting this miR-27b/Snail1 axis as putative target for the therapeutic treatment of NSCLC.
HEADING AIMS: MicroRNA-27b (miR-27b) has been shown to play a role in the progression of many different forms of cancer, but its specific relevance in the context of non-small cell lung cancer (NSCLC) remains uncertain. As such, this study sought to explore the role of miR-27b in NSCLC and the mechanisms whereby it functions. MATERIALS AND METHODS: We quantified miR-27b and target gene expression via quantitative real-time PCR (RT-qPCR).We then used functional including proliferation assays, migration assay, flow cytometry, and western blotting to explore the mechanisms whereby miR-27b functions in vitro and in vivo. We additionally confirmed miR-27b target genes via luciferase reporter assay. KEY FINDINGS: We observed a marked decrease in miR-27b expression in NSCLC patient samples relative to paracancerous control tissues. We further found that altering miR-27b expression levels in vitro affected NSCLC tumor cell migration, proliferation, and ability to undergo epithelial-mesenchymal transition. Through the use of target prediction algorithms we identified Snail to be a miR-27b target protein that was suppressed when this miRNA was highlight expressed. Lastly, we found miR-27b expression to increase NSCLC cell sensitivity to cisplatin through its ability to target Snail. SIGNIFICANCE: Our results clearly demonstrate that miR-27b can suppress NSCLC tumor development and progression, highlighting this miR-27b/Snail1 axis as putative target for the therapeutic treatment of NSCLC.