Background Lung cancer (LC) remains a leading cause of cancer-related mortality worldwide. Long noncoding RNAs (lncRNAs) are crucial regulatory molecules in diverse pathological processes, including cancer progression. This study was conducted to probe the influence of lncRNA HAGLR on the growth, metastasis and stemness of LC cells. Methods Aberrantly expressed lncRNAs in LC tissues were screened out using microarray analysis. HAGLR expression in LC tissues and cells and in the paired normal ones was determined using RT-qPCR. Overexpression of HAGLR was administrated in H1299 and A549 cells to identify its function in the biological characteristics of LC cells. Sub-cellular localization of HAGLR was determined, and the downstream molecules involved in the HAGLR-mediated events were predicted on a bioinformation system and validated through dual luciferase reporter gene assay. Results HAGLR was poorly expressed in both LC tissues and cells. Overexpression of HAGLR inhibited viability, proliferation and metastasis, and reduced the stemness of H1299 and A549 cells. HAGLR up-regulated SLC34A2 expression through sponging miR-330-3p, leading to further inactivation of the Wnt/β-catenin signaling pathway. Artificial activation of the Wnt/β-catenin pathway recovered the viability and promoted metastasis of LC cells inhibited by HAGLR Conclusion HAGLR serves as a competing endogenous RNA for miR-330-3p to upregulate miR-330-3p expression and inactivate the Wnt/β-catenin pathway, leading to inhibited growth and metastasis and reduced stemness of LC cells.