We investigated the effects of lncRNA PCGEM1 on the tumorigenesis and development of endometrial carcinoma (EC) and its possible molecular mechanism. We found that PCGEM1 expression was significantly higher in EC tissues than in normal endometrial tissues via quantitative reverse transcription (qRT)-PCR. The upregulation of PCGEM1 promoted the proliferation, migration, and invasive ability of EC cells while inhibiting apoptosis. The silencing of PCGEM1 had the opposite effects. Nude mouse xenograft assay showed that PCGEM1 overexpression could promote tumor growth in vivo . Western blotting and immunohistochemistry showed that PCGEM1 also upregulated STAT3 expression, which affected the expression of B-cell lymphoma-2, survivin, vascular endothelial growth factor A, and matrix metalloproteinase-2. Furthermore, the dual-luciferase reporter assay confirmed that miR-129-5p could bind directly to both PCGEM1 and STAT3. In addition, qRT-PCR showed that overexpression of PCGEM1 caused a decrease in miR-129-5p expression, and silencing of PCGEM1 produced the opposite result. In the PCGEM1 -overexpressing cells, overexpression of miR-129-5p reduced the expression of STAT3 at both mRNA and protein levels. Thus, we confirmed that PCGEM1 could upregulate the expression of STAT3 by acting as a competing endogenous RNA for miR-129-5p, thereby affecting the occurrence and development of EC.