In vitro experiments showed that higher expression of SNHG14 led to higher cell proliferation, migration and invasion, while miR-186 significantly inhibited these tumor phenotypes.
SNHG14 contributed to cell proliferation, migration and invasion, while suppressed apoptosis in CRC cells by targeting miR-944/KRAS axis through PI3K/AKT pathway, representing novel biomarkers for CRC therapy.
Our study uncovers a new oncogene in BC and suggests that SNHG14 could enhance BC cell proliferation and invasion via sponging miR-193a-3p, which provided a novel therapeutic target for BC patients.