Long non-coding RNA LINC00511 regulates the expression of microRNA-625-5p and activates signal transducers and activators of transcription 3 (STAT3) to accelerate the progression of gastric cancer

Abstract

This study aimed to investigate the expression, biological function, and downstream mechanism of LINC00511 in gastric cancer (GC). In paired GC samples, LINC00511, miR-625-5p and STAT3 mRNA expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR); STAT3 protein expression was detected by immunohistochemical (IHC). The gain-of-function and loss-of-function models were established, and the proliferative and migrative ability of GC cells were measured by CCK-8 and transwell assays, respectively. The regulatory relationship between miR-625-5p and LINC00511 or STAT3 was examined by bioinformatics analysis, luciferase reporter gene assay, qRT-PCR, and western blot. We reported that LINC00511 and STAT3 expressions in GC tissues and cell lines were observably up-regulated, while miR-625-5p expression was inhibited. High expression of LINC00511 could facilitate the proliferation and promote the migration of GC cells. miR-625-5p was proved to be a downstream target of LINC00511, and LINC00511 could induce the expression of STAT3 by inhibiting the expression of miR-625-5p. Additionally, knockdown of LINC00511 suppressed the growth and lung metastases of CRC cells in nude mice. In conclusion, LINC00511 promotes the GC cell proliferation and migration via targeting the miR-625-5p/STAT3 axis, implying that LINC00511 can function as a target for GC therapy.

Keywords

• gastric cancer
• linc00511
• mir-625-5p
• stat3