LINC00324 exerts tumor-promoting functions in lung adenocarcinoma via targeting miR-615-5p/AKT1 axis.

OBJECTIVE

The underlying mechanism of long non-coding RNA (lncRNA) in lung adenocarcinoma (LAC) has not been fully understood yet. Hence, this study aimed to determine the biological function of LINC00324 in LAC and to provide a novel diagnostic and therapeutic target for it.

PATIENTS AND METHODS

The expression level of LINC00324 in 87 paired LAC tumor tissues and matched para-tumor tissues was detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was employed to analyze the cell proliferative ability, whereas flow cytometry was performed to detect cell apoptotic rate. Cell metastasis change was measured using wound-healing assay and transwell assay. Luciferase reporter gene assay and Western blotting analysis were utilized to investigate the underlying mechanism of LINC00324 in LAC.

RESULTS

LINC00324 was highly expressed in LAC tissues compared with the para-tumor samples. Identically, the expression level of LINC00324 was significantly higher in LAC cell lines. The overexpression of LINC00324 promoted cell proliferation and inhibited cell apoptosis of LAC cells, while knockdown of LINC00324 presented the opposite effect. Up-regulation of LINC00324 accelerated cell migration and invasion, but down-regulation of LINC0324 decreased cell metastasis of LAC cells. Furthermore, miR-615-5p was found to be regulated by LINC00324 and inhibited AKT1 expression, indicating that LINC00324 promoted cell progression via affecting the miR-615-5p/AKT1 pathway.

CONCLUSIONS

LINC00324 was significantly over-expressed in LAC tissues and cells. It promoted proliferation and metastasis but inhibited cell apoptosis of LAC cells via sponging miR-615-5p to promote AKT1 expression. Our results demonstrated LINC00324 as a novel diagnostic and therapeutic target for LAC.