Endometrial cancer (EC) is an aggressive tumor in females and the development of EC is considered to regulate by some long non-coding RNAs (lncRNAs). Therefore, this study aimed to investigate the regulatory mechanism of lncRNA LINC01106 on EC. Methods: The expression of lncRNA LINC01106, miR-449a and MET in EC tissues and cells was detected by qRT-PCR. Through MTT, wound healing and transwell invasion assays, the proliferation, migration and invasion of EC cells were detected, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibiting effect of LINC01106 knockdown on EC in vivo. The interactions between miR-449a and LINC01106/ MET were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein level of MET. Results: LncRNA LINC01106 expression was highly up-regulated in EC tissues and cells. The proliferation, migration and invasion of EC cells in vitro were inhibited by the transfection of sh-LINC01106. The growth of tumor xenograft was suppressed by injection of sh-LINC01106. MiR-449a was a target of LINC01106and was negatively modulated by LINC01106. MiR-449a overexpression suppressed the proliferation, migration and invasion of EC cells. In addition, MET was identified as a target gene of miR-449a. Both the high expression of miR-449a and low expression of MET reversed the inhibiting effects of LINC01106 knockdown on Ishikawa cells. Conclusion: Silencing of LINC01106 inhibits the occurrence and development of EC via regulating the miR-449a/MET axis. This study provides a possible therapeutic strategy for EC.