LINC00941 promotes proliferation and metastasis of pancreatic adenocarcinoma by competitively binding miR-873-3p and thus upregulates ATXN2.

OBJECTIVE

Globally, the incidence and mortality of pancreatic adenocarcinoma (PAAD) have constantly increased. Long non-coding RNAs (lncRNAs) are considered as vital regulators in human cancers. This study aims to elucidate the role of LINC00941 in regulating PAAD progression and the molecular mechanism.

PATIENTS AND METHODS

Through database analyses, the expression pattern of LINC00941 in PAAD tissues and its prognostic value were uncovered. Its level in PAAD cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). After knockdown of LINC00941, proliferative and metastatic rates in BxPC-3 and PANC-1 cells were examined by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay, respectively. The axis of LINC00941/miR-873-3p/ATXN2 was tested by Dual-Luciferase reporter assay and Pearson correlation test.

RESULTS

LINC00941 was abnormally upregulated in PAAD tissues, and linked to the prognosis. Knockdown of LINC00941 inhibited proliferative, migratory and invasive abilities in BxPC-3 and PANC-1 cells. MiR-873-3p was the target gene binding LINC00941, which was downregulated in PAAD tissues. Overexpression of miR-873-3p inhibited proliferative, migratory and invasive abilities in BxPC-3 and PANC-1 cells, and the inhibited trends were abolished by co-overexpression of LINC00941. Furthermore, ATXN2 was confirmed to be the target gene binding miR-873-3p, which was upregulated in PAAD tissues. It was negatively correlated to miR-873-3p and positively correlated to LINC00941.

CONCLUSIONS

LINC00941 is upregulated in PAAD tissues. It stimulates PAAD to proliferate and metastasize by competitively binding miR-873-3p and thus upregulates ATXN2.