Abstract
Colorectal cancer is a common cause of cancer-related death worldwide. Thus, there is an urgent need to determine the mechanism of progression of colorectal cancer. In this study, we investigated the function and mechanism of long non-coding RNA LINC00958, providing a new biomarker for colorectal cancer. The expression of LINC00958, miR-3064-5p, and LEM domain containing 1 (LEMD1) in colorectal cancer tissues and cell lines was analyzed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). The interaction between LINC00958, miR-3064-5p, and LEMD1 was assessed using the luciferase assay. The viability, proliferation, migration, invasion, and apoptosis of colorectal cancer cells with silenced LINC00958, miR-3064-5p, and LEMD1 were investigated using the cell counting kit-8 (CCK-8), 5'-Bromo-2'-deoxyuridine (BrdU), flow cytometry, wound healing, and transwell assays. Phosphorylated phosphoinositide 3-kinase (p-PI3K) and phosphorylated protein kinase B (p-AKT) protein levels were measured by western blotting. LINC00958 and LEMD1 were found to have increased, while the expression of miR-3064-5p was decreased in colorectal cancer tissues and cell lines. Silencing of LINC00958 hampered cell viability, proliferation, migration, and invasion, while enhancing the apoptosis in colorectal cancer cells. Notably, LINC00958 inhibited miR-3064-5p and promoted LEMD1; the miR-3064-5p inhibitor abrogated the effect of LINC00958 silencing in colorectal cancer cells. Additionally, LEMD1 knockdown inhibited the activation of PI3K/AKT signaling. Our analyses have shown that LINC00958 could facilitate the progression of colorectal cancer by sponging miR-3064-5p and releasing LEMD1, leading to the activation of the PI3K/AKT pathway. Thus, LINC00958 may be considered as an effective biomarker for the treatment of colorectal cancer.