Long noncoding RNA LINC00173 is downregulated in cervical cancer and inhibits cell proliferation and invasion by modulating the miR-182-5p/FBXW7 axis |
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| Affiliation: | 1. Department of Gynecologic Oncology, Shaanxi Provincial Tumor Hospital, Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, 710061, China;2. Department of Nursing, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710061, China;1. Institute of Reproductive & Stem Cell Engineering, School of Basic Medicine Science, Central South University, Changsha, 410000, China;2. Reproductive & Genetic Hospital of CITIC-Xiangya, Changsha, 410000, China;3. Department of Urology, Hunan Cancer Hospital, Changsha, 410000, China;1. Howard Hughes Medical Institute and Department of Pathology, NYU School of Medicine, New York, NY 10016, USA;2. NYU Cancer Institute and Helen L. and Martin S. Kimmel Center for Stem Cell Biology, NYU School of Medicine, New York, NY 10016, USA;1. Department of Urology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 250021, PR China;2. Department of Center Laboratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 250021, China;1. The Key Laboratory of Molecular Diagnosis in Laboratory Medicine, Department of Pathogenobiology, Daqing Branch of Harbin Medical University, Daqing 163319, China;2. Department of General Surgery of Fifth Clinical Hospital of Harbin Medical University, Daqing 163319, China |
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| Abstract: | Accumulating evidence has supported the concept that long noncoding RNAs (lncRNAs) participate in the initiation and progression of human cervical cancer (CC). The long intergenic nonprotein-coding RNA 173 (LINC00173) is a recently identified cancer-associated factor. However, the expression and biological role of LINC00173 in CC are poorly understood. Here, for the first time, we found that the expression of LINC00173 was decreased in CC tissues compared with that in nontumor tissues. Data from The Cancer Genome Atlas (TCGA) further revealed that the downregulated expression of LINC00173 in CC tissues was correlated with poor survival. Functionally, LINC00173 overexpression suppressed HeLa cell proliferation via induction of G0/G1 phase arrest. Ectopic expression of LINC00173 also repressed the invasiveness of HeLa cells. Conversely, LINC00173 depletion resulted in the enhanced proliferation and invasiveness of C33A cells. Mechanistically, LINC00173 functioned as a molecular sponge for miR-182-5p and inversely regulated the miR-182-5p level in CC cells. F-box and WD repeat domain-containing 7 (FBXW7) was identified as the target of miR-182-5p. LINC00173 overexpression enhanced the FBXW7 level via regulation of miR-182-5p in HeLa Cells. More importantly, the inhibitory effects of LINC00173 on HeLa cell proliferation and invasiveness were reversed by FBXW7 silencing. Taken together, the results indicate that the LINC00173/miR-182-5p/FBXW7 axis is critical for CC progression, which might offer new insights into effective therapy for CC. |
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| Keywords: | Cervical cancer Long noncoding RNA microRNA FBXW7 Tumor progression |
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