<p>The Long Noncoding RNA Linc01833 Enhances Lung Adenocarcinoma Progression via MiR-519e-3p/S100A4 Axis</p>

Abstract

Introduction Lung cancer (LC) is among the most prevalent malignancies worldwide, with extremely high morbidity and mortality rates. Mounting evidence has suggested that the abnormally expressed long noncoding RNA (lncRNA) in lung cancer tissues may play vital roles in tumor progression. In the present research, we aimed to examine the functions and underlying mechanism of linc01833 in lung adenocarcinoma (LUAD). Methods qRT-PCR was employed to determine transfection efficiency. CCK-8, transwell invasion assay, Western blotting analysis and qRT-PCR were used to detect proliferation as well as migration of different LUAD cell lines, and were also applied to determine the changes during epithelial–mesenchymal transformation (EMT). Afterwards, bioinformatics and dual-luciferase reporter assay were utilized to explore and to identify the potential corresponding targets of linc01833 and miR-519e-3p. Results Linc01833 OE can significantly improve proliferation as well as invasion ability of LC cells and promote the EMT process. Dual-luciferase reporter assay demonstrated that linc01833 could directly bind to miR-519e-3p, thereby inhibiting its expression. Further experiments showed that S100A4 was a direct target of miR-519e-3p. Rescue assay demonstrated that linc01833 acted on the miR-519e-3p/S100A4 axis. Conclusion We verified the mechanism of linc01833 in promoting infiltration and metastasis in LUAD. To be specific, linc01833 can function as a competitive endogenous RNA (ceRNA) to adsorb miR-519e-3p through a sponge and regulate S100A4 in lung cancer, thereby being involved in LUAD progression. Collectively, our research provides new insights towards the in-depth understanding of LC progression mechanisms.

Five long non-coding RNAs establish a prognostic nomogram and construct a competing endogenous RNA network in the progression of non-small cell lung cancer

“…Jiang et al discovered that BANCR was able to moderate the ability of invasion and metastasis in lung cancer through the p38 MAPK and JNK pathway rather than the ERK MAPK pathway [ 43 ]. LINC01833 was demonstrated to promote the infiltration and metastasis of LUAD by adsorbing miR-519e-3p through a sponge and regulate S100A4 expression [ 44 ]. FAM83A-AS1 was proved to enhance cell migration, invasion and EMT by modulating the miR-150-5p/MMP14 pathway [ 45 ].…”

Construction and analysis of the ceRNA network hsa_circ_0031968/miR-3611/GCG in lung adenocarcinoma

“…Circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) are prominent members of non-coding RNAs (ncRNAs) and play vital roles in all aspects of human cancer through gene regulation (6). Our team's previous research focused on the regulatory mechanism of the ceRNA regulatory network involved in lncRNA in LUAD, and we have confirmed that the Linc01833/miR-519e-3p/S100A4 axis can significantly promote the proliferation, invasion and metastasis of LUAD (7). There are not many studies on the mechanism of the ceRNA regulatory network involved in circRNA in LUAD.…”

MCM3AP‑AS1 promotes cisplatin resistance in gastric cancer cells via the miR‑138/FOXC1 axis

“…Previous studies have reported that lncRNAs may act as ceRNAs by sponging miRNAs to release downstream mRNAs ( 36 – 38 ). FOXC1, a member of the FOX transcription factor family, serves a vital role in numerous types of cancer, such as colorectal, non-small cell lung and prostate cancer ( 39 – 41 ).…”