Supplementary material from "MALAT1 promotes gastric adenocarcinoma through MALAT1-miR-181a-5p-AKT3 axis"

Gastric adenocarcinoma, originating from the gastric mucosal epithelium, has the highest incidence rate among various malignant tumours in China. As a crucial lncRNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been suggested to play important roles in many tumours. Here, we aimed to investigate the role and underlying mechanism of MALAT1 in gastric adenocarcinoma. qRT-PCR was applied to determine the expression levels of MALAT1 in serum and cell lines. Cck-8 assay and clonogenic survival assay were used to examine cell proliferation and apoptosis. Protein level of RAC-γ serine/threonine-protein kinase (AKT3) was determined by western blot. Our results showed that MALAT1 was highly expressed in the serum of gastric adenocarcinoma patients and cell lines. Downregulating MALAT1 inhibited proliferation and promoted apoptosis of MGC-803 cells. In addition, MALAT1 directly targeted and decreased the expression of miR-181a-5p, which in turn upregulated the expression of AKT3. Further, overexpressing miR-181a-5p or directly inhibiting the AKT pathway with an inhibitor Ipatasertib exhibited similar effects as MALAT1 knockdown. Our research proposes a novel mechanism where the role of MALAT1 is dependent on the MALAT1-miR-181a-5p-AKT3 axis. MALAT1 competes with AKT3 for miR-181a-5p binding, thereby upregulating AKT3 protein level and ultimately promoting the growth of gastric adenocarcinoma.