LINC00467 facilitates osteosarcoma progression by sponging miR‑217 to regulate KPNA4 expression
- Jing Yan
- Tao Fang
- Ming Zhang
- Quan Zhou
Affiliations: Department of Orthopaedics, The Affiliated Huaian Hospital of Xuzhou Medical University, Huaian, Jiangsu 223002, P.R. China
- Published online on: January 26, 2021 https://doi.org/10.3892/ijmm.2021.4859
Copyright: © Yan
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Osteosarcoma (OS) is a musculoskeletal malignancy that originates from interstitial cells. An increasing number of studies have verified that long non‑coding RNAs (lncRNAs) participate in the progression of numerous types of cancer. It has been reported that LINC00467 is a cancer‑promoting gene in some types of cancer; however, the regulatory mechanism of LINC00467 in OS remains unknown. In the present study, reverse transcription-quantitative PCR was used to determine LINC00467 expression in OS tissues and cells. Additionally, the impact of LINC00467‑knockdown on OS cell proliferation, migration and invasion was analyzed using Cell Counting Kit‑8, colony formation and Transwell assays, as well as western blot analysis. RNA pulldown and luciferase reporter assays were conducted to investigate the regulatory mechanism of LINC00467 in OS. The results delineated that LINC00467 expression was elevated in OS tissues and cells, and that high LINC00467 expression was associated with a poor prognosis in patients with OS. LINC00467 inhibition suppressed OS progression by inhibiting cell proliferation, migration, invasion and epithelial‑mesenchymal transition. LINC00467 served as a molecular sponge for microRNA (miR)‑217, while karyopherin subunit α4 (KPNA4) was a downstream target gene of miR‑217. Moreover, the overexpression of KPNA4 reversed the inhibitory effects of LINC00467 inhibition on OS progression. Therefore, the present study elucidated the potential mechanism of LINC00467 in OS and indicated that LINC00467 exerted its carcinogenic effects on OS through the miR‑217/KPNA4 axis, implying that LINC00467 may be a novel potential therapeutic target for OS.