LncRNA GASL1 inhibits tumor growth in gastric carcinoma by inactivating the Wnt/β‑catenin signaling pathway
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- Published online on: March 18, 2019 https://doi.org/10.3892/etm.2019.7409
- Pages: 4039-4045
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Copyright: © Peng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Growth arrest associated lncRNA 1 (GASL1) is a newly discovered tumor suppressor long non‑coding RNA (lncRNA) in osteosarcoma; however its role in other malignancies remains unknown. The aim of the present study was to investigate the involvement of GASL1 in gastric cancer. In the current study, gastric cancer tissue and adjacent healthy tissue samples were collected from patients with gastric carcinoma, and blood samples were collected from patients with gastric carcinoma and healthy controls to detect the expression of serum GASL1. All patients were followed up for 5 years and the diagnostic and prognostic value of GASL1 for gastric carcinoma was evaluated by ROC and survival curve analyses, respectively. The chi‑square test was used to analyze the correlation between serum levels of GASL1 and the clinicopathological features of patients with gastric carcinoma. A GASL1 expression vector and GASL1 small interfering RNA were transfected into gastric cancer cell lines and the effects on β‑catenin expression and cell proliferation were examined by western blot and cell proliferation assays, respectively. The expression level of lncRNA GASL1 was significantly downregulated in gastric cancer tissues compared with adjacent normal tissues from patients with gastric carcinoma. In addition, serum levels of GASL1 were significantly decreased in patients with gastric carcinoma when compared with healthy controls. Serum GASL1 levels distinguished patients with gastric carcinoma from healthy controls, and low expression levels of GASL1 were associated with decreased postoperative survival time. GASL1 overexpression downregulated, while GASL1 knockdown upregulated β‑catenin expression. GASL1 overexpression inhibited, and GASL1 knockdown promoted gastric cancer cell proliferation. In addition, treatment with a Wnt agonist demonstrated no significant effect on GASL1 expression, however the inhibitory effect of GASL1 overexpression on cell proliferation was reduced following treatment with the Wnt agonist. In conclusion, the GASL1 lncRNA may inhibit tumor growth in patients with gastric carcinoma by inactivating the Wnt/β‑catenin signaling pathway.
