LINC00689 induces gastric cancer progression via modulating the miR‐338‐3p/HOXA3 axis

Abstract Background LINC00689 acts one critical regulatory role in several tumors. However, the functional, regulatory mechanism and expression of LINC00689 remains unknown in gastric cancer. Methods LINC00689 and miR‐338‐3p levels were determined using a quantitative reverse transcriptase‐polymerase chain reaction analysis and an enzyme‐linked immunoassay and a cell‐counting kit‐8 assay were utilized to detect interleukin (IL)‐8, IL‐6 and IL‐1β expression and cell proliferation, respectively. Results We found that LINC00689 and HOXA3 are overexpressed and miR‐338‐3p is decreased in gastric cancer cells. Compared to control specimens, LINC00689 is overexpressed in gastric cancer specimens and the level of LINC00689 was up‐regulated in 32 cases (32/40; 80.0%) compared to control samples. LINC00689 increased cell growth, epithelial–mesenchymal transition (EMT) development and secretion of inflammatory factors in gastric cancer. Compared to control specimens, miR‐338‐3p expression was decreased in gastric cancer specimens and a Pearson's correlation assay revealed that miR‐338‐3p was negatively correlated with LINC00689 expression in gastric cancer specimens. HOXA3 was identified as one target gene of miR‐338‐3p and Ectopic expression of LINC00689 suppressed miR‐338‐3p and enhanced HOXA3 expression in HGC‐27 cells. LINC00689 enhanced cell growth, EMT development and secretion of inflammatory factors by promoting HOXA3. Conclusions LINC00689 may present a potential future target for gastric cancer treatment.