Long Non-coding RNA LINC01503 Promotes Gastric Cancer Cell Proliferation and Invasion by Regulating Wnt Signaling

Background Previous studies have indicated that the dysregulation of long non-coding RNAs plays an important role in tumors. LINC01503 is a newly discovered lncRNA that promotes development of various tumor types. However, the function of LINC01503 in gastric cancer has not been reported yet. Aims T...

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Veröffentlicht in:Digestive diseases and sciences 2021-02, Vol.66 (2), p.452-459
Hauptverfasser: Ding, Jian, Shi, Feng, Xie, Guangdong, Zhu, Yong
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Sprache:eng
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Zusammenfassung:Background Previous studies have indicated that the dysregulation of long non-coding RNAs plays an important role in tumors. LINC01503 is a newly discovered lncRNA that promotes development of various tumor types. However, the function of LINC01503 in gastric cancer has not been reported yet. Aims To explore the function of LINC01503 in gastric cancer development and the underlying molecular biological regulatory mechanisms. Methods LINC01503 expression in tissues and cell lines of gastric cancer were determined through qRT-PCR. Transwell assay and cell number counting experiments were employed to detect the cell invasion and proliferation. C-myc, cyclin D1, and β-catenin expressions were analyzed through Western blot and qRT-PCR. Results LINC01503 was highly expressed in gastric cancer tissues and cell lines, which was correlated with poor prognosis. Knockdown of LINC01503 suppressed gastric cancer cell proliferation and invasion, whereas overexpression of LINC01503 showed a reverse trend. Silencing LINC01503 significantly inhibited the expression of c-myc, cyclin D1, and β-catenin. Overexpressing β-catenin rescued the inhibitory effects, induced by LINC01503 silencing, on gastric cancer cell proliferation and metastasis. Conclusions This research reported that the elevated expression of LINC01503 could promote proliferation and metastasis of gastric cancer through positively regulating the Wnt/β-catenin pathway.
ISSN:0163-2116
1573-2568
DOI:10.1007/s10620-020-06215-4