ABSTRACT
Objective@#The purpose of this study is to explore the biological function of long non-coding RNA (lncRNA) HMMR-AS1 in proliferation and metastasis of lung adenocarcinoma (LUAD). @*Methods@#Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of HMMR-AS1 and its sense strand HMMR in LUAD cell lines. Then we knock down the HMMR-AS1 expression through small interfering RNA and evaluate the transfection efficiency and its effect on the expression of HMMR. CCK-8 (cell counting kit), clone formation, flow cytometric analysis, wound scratch assay and transwell assay were used to assess the biological function of A549 and H1299 cells. Western blot was used to detect the protein expression of HMMR in the two cell lines after transfection with si-HMMR-AS1. @*Results@#The expression of HMMR-AS1 in A549 and H1299 cells of LUAD cell line was markedly higher than that in normal lung epithelial cell BEAS-2A by upregulating approximately 3.06 and 5.02 folds (P＜0.05), respectively. After transfection with si-HMMR-AS1, the expression of HMMR-AS1 markedly reduced in both levels of transcription and protein (P＜0.05). Furthermore, knocking down of HMMR-AS1 significantly inhibited the proliferation, migration and invasion abilities, and increased the apoptosis rates of A549 and H1299 cells. @*Conclusion@#LncRNA HMMR-AS1 could promote malignant progression of LUAD cells through enhancing the growth, migration and invasion ability of LUAD cells.