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lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis

  • Authors:
    • Wei Yu
    • Yong Dai
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China
    Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 624
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    Published online on: June 29, 2021
       https://doi.org/10.3892/ol.2021.12885
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Abstract

Liver cancer is becoming one of the most lethal malignancies due to its high incidence and mortality. Accumulating studies have indicated that long non‑coding RNAs (lncRNAs) are critical regulators of the tumorigenesis and development of various types of cancer, including liver cancer. LncRNA LOXL1‑antisense RNA 1 (LOXL1‑AS1) has been identified as an oncogene in some types of human cancer; however, its role in liver cancer remains obscure. Reverse transcription‑quantitative PCR was used to measure LOXL1‑AS1 expression in liver cancer tissues and cells. Western blot, MTT, colony formation, glucose uptake and wound healing assays were used to explore the biological function of LOXL1‑AS1 in liver cancer cells. Bioinformatics analysis and RNA pull‑down and luciferase reporter assays were used to explore the molecular mechanism of LOXL1‑AS1 in liver cancer cells. Statistical analysis was used to compare the experimental results of different groups. In the present study, LOXL1‑AS1 expression was significantly upregulated in liver cancer tissues and cells compared with in normal liver tissues and cells, respectively. High LOXL1‑AS1 expression was associated with poor clinical outcomes in patients with liver cancer. Furthermore, LOXL1‑AS1‑knockdown suppressed glucose metabolism, proliferation, migration and epithelial‑mesenchymal transition (EMT) of liver cancer cells. Subsequently, LOXL1‑AS1 acted as a microRNA (miR)‑377‑3p sponge, and nuclear factor I B (NFIB) was confirmed as the downstream target of miR‑377‑3p in liver cancer cells. Additionally, rescue assays suggested that NFIB overexpression countervailed the inhibitory influence of LOXL1‑AS1 silencing on liver cancer cellular processes. The present study demonstrated that LOXL1‑AS1 promoted glucose metabolism, proliferation, migration and EMT of liver cancer cells by sponging miR‑377‑3p and modulating NFIB, which may provide a novel insight for the treatment of liver cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Yu W and Dai Y: lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis. Oncol Lett 22: 624, 2021.
APA
Yu, W., & Dai, Y. (2021). lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis. Oncology Letters, 22, 624. https://doi.org/10.3892/ol.2021.12885
MLA
Yu, W., Dai, Y."lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis". Oncology Letters 22.2 (2021): 624.
Chicago
Yu, W., Dai, Y."lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis". Oncology Letters 22, no. 2 (2021): 624. https://doi.org/10.3892/ol.2021.12885
Copy and paste a formatted citation
x
Spandidos Publications style
Yu W and Dai Y: lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis. Oncol Lett 22: 624, 2021.
APA
Yu, W., & Dai, Y. (2021). lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis. Oncology Letters, 22, 624. https://doi.org/10.3892/ol.2021.12885
MLA
Yu, W., Dai, Y."lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis". Oncology Letters 22.2 (2021): 624.
Chicago
Yu, W., Dai, Y."lncRNA LOXL1‑AS1 promotes liver cancer cell proliferation and migration by regulating the miR‑377‑3p/NFIB axis". Oncology Letters 22, no. 2 (2021): 624. https://doi.org/10.3892/ol.2021.12885
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