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LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis

  • Authors:
    • Xuanyu Chen
    • Song Chen
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 8
    |
    Published online on: February 1, 2021
       https://doi.org/10.3892/or.2021.7959
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Abstract

The aim of the present study was to explore the effects of LINC00649 on the proliferation, migration and invasion of bladder cancer (BC) and identify possible mechanisms. Through TCGA database analysis of LINC00649 expression in bladder cancer and the association of LINC00649 with the BC patient prognosis, RT‑qPCR was employed for detecting LINC00649 expression in 60 clinical tissue specimens and cell lines of bladder cancer. The lentivirus stable transfection or small interfering RNA was used to increase or decrease the LINC00649 expression level in T24 and UM‑UC‑3 cells. CCK8 and clone formation assay were utilized to observe the effects of LINC00649 on the proliferation and colony formation of BC cells. Transwell experiment was performed to detect the effects of LINC00649 on the migration and invasion of bladder cancer. Bioinformatics database was used to identify the possible downstream targets of LINC00649 while RT‑qPCR, western blot analysis and dual luciferase reporter gene experiments were carried out to verify the possible molecular mechanism. The TCGA database analysis revealed a significantly high expression of LINC00649 in bladder cancer and an association of LINC00649 expression with overall survival rate of BC patients. As shown by RT‑qPCR detection, LINC00649 expression was notably upregulated in BC tissues and BC cell lines. In addition, statistical analyses unveiled that highly expressed LINC00649 was clearly associated with poor overall survival of bladder cancer. Based on the in vitro cell experiment, upregulated LINC00649 considerately enhanced the proliferation, migration and invasion of BC cells, as opposed to those in T24 and UM‑UC‑3 cells by suppressing LINC00649. Mechanically, LINC00649 may promote the malignant progression of bladder cancer by regulating miR‑15a‑5p to promote the HMGA1 expression axis. Overall, LINC00649 upregulates HMGA1 expression by binding to miR‑15a‑5p to enhance the proliferation, migration and invasion of BC cells. Thus, LINC00649 is a potential biomarker and therapeutic target for bladder cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Chen X and Chen S: LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis. Oncol Rep 45: 8, 2021.
APA
Chen, X., & Chen, S. (2021). LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis. Oncology Reports, 45, 8. https://doi.org/10.3892/or.2021.7959
MLA
Chen, X., Chen, S."LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis". Oncology Reports 45.4 (2021): 8.
Chicago
Chen, X., Chen, S."LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis". Oncology Reports 45, no. 4 (2021): 8. https://doi.org/10.3892/or.2021.7959
Copy and paste a formatted citation
x
Spandidos Publications style
Chen X and Chen S: LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis. Oncol Rep 45: 8, 2021.
APA
Chen, X., & Chen, S. (2021). LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis. Oncology Reports, 45, 8. https://doi.org/10.3892/or.2021.7959
MLA
Chen, X., Chen, S."LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis". Oncology Reports 45.4 (2021): 8.
Chicago
Chen, X., Chen, S."LINC00649 promotes bladder cancer malignant progression by regulating the miR‑15a‑5p/HMGA1 axis". Oncology Reports 45, no. 4 (2021): 8. https://doi.org/10.3892/or.2021.7959
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