LINC00342 regulates cell proliferation, apoptosis, migration and invasion in colon adenocarcinoma via miR-545-5p/MDM2 axis

Abstract

Aim: Colon adenocarcinoma (COAD) is the third most common cancer in the world. We aimed to explore the functional mechanism of LINC00342 in COAD.

Methods: The LINC00342 expressions in COAD tissues were detected via qRT-PCR and in situ hybridization analysis. Statistical analysis was performed to analyze the relationship between LINC00342 expression and COAD clinical features. Small interfering LINC00342 (siLINC00342)/siCtrl were synthesized and then transfected into COAD cells. Cell apoptosis and proliferation were respectively assessed by flow cytometry and cell counting kit-8 assay. Cell migration and invasion were both measured using transwell assay. The target miRNA of LINC00342 were predicted and verified by online bioinformatics tools and luciferase reporter assay and RNA pull-down assay. Mice COAD models were constructed to explore the effects of LINC00342 on COAD in vivo.

Results: LINC00342 was over-expressed in COAD tissues and LINC00342 overexpression was related to the poor prognosis of COAD patients. LINC00342 knockdown inhibited cell proliferation, migration and invasion and promoted apoptosis of COAD cells. LINC00342 targeted to miR-545-5p/murine double minute 2 (MDM2) in COAD. In COAD tissues and cell lines, LINC00342 expression was positively correlated to MDM2 expression, while it was negatively correlated to miR-545-5p expression. Both miR-545-5p-mimic and siMDM2 transfection could recover the changes of cell biological activities which were induced by LINC00342 overexpression. LINC00342 knockdown suppressed COAD tumor growth in vivo.

Conclusion: LINC00342 affected cell biological activities of COAD in vivo and in vitro via regulating miR-545-5p/MDM2. It might a novel target in COAD therapy.

Keywords: Animal model; Colon adenocarcinoma; LIN00342; MDM2; miR-545-5p.