Published online Apr 15, 2020. doi: 10.4251/wjgo.v12.i4.394
Peer-review started: December 21, 2019
First decision: January 19, 2020
Revised: February 4, 2020
Accepted: March 22, 2020
Article in press: March 22, 2020
Published online: April 15, 2020
Processing time: 116 Days and 4.1 Hours
It has been reported that LINC00511 contributes to tumorigenesis in various diseases. However, the role of LINC00511 in gastric cancer (GC) cell growth remains mostly unknown.
The specific biological function and regulatory mechanism of LINC00511 in GC have not been extensively explored.
In this study, the authors aimed to determine whether the long noncoding RNAs LINC00511 exerted its carcinogenic function in GC via the miR-124-3p/PDK4 axis.
The cell culture and transfection, RNA extraction and quantitative real-time PCR, CCK-8 assay, Colony formation assay, Luciferase reporter assay, RIP assay, RNA pull-down assay, and Western blot analysis were used to show expression and mechanisms of LINC00511 in GC progression and apoptosis. Rescue assays were performed to verify the relationships among LINC00511, miR-124-3p and PDK4 further.
The expression of LINC00511 was remarkably upregulated in GC cells compared to that in corresponding normal cell lines. Compared to the controls, cell proliferation was inhibited, and cell apoptosis was increased upon LINC00511 knockdown, demonstrating that LINC00511 influenced GC cell growth. An exploration of the molecular mechanism revealed that LINC00511 functioned as a molecular sponge of miR-124-3p and that PDK4 was a downstream target of miR-124-3p in GC.
The results of the study demonstrate that LINC00511 promotes gastric cancer cell growth by acting as a ceRNA to regulate the miR-124-3p/PDK4 axis, which may be a promising therapeutic target for GC.