Objective: Endometrial cancer (EC) is a common gynecologic malignancy; myometrial invasion (MI) is a typical approach of EC spreads and an important index to assess tumor metastasis and outcome in EC patients. CCT7 is a member of the TCP1 chaperone family, involved in cytoskeletal protein folding and unfolding. In this study, the role of CCT7 in EC development was investigated. Methods: Clinical data for 87 EC cases and expression of CCT7 were analyzed. CCT7 was knocked out using siRNA- CCT7 in Ishikawa and RL95-2 cells, and their function about proliferation, apoptosis, and invasion was further tested. Bioinformatics methods were used to predict the potential pathways of CCT7 in EC development. Results: The rates of CCT7-positive cells in EC and adjacent normal endometrium tissues had a significant difference (67.8 vs. 51.4%, p = 0.035), and the expression rate increased from low to high pathological stage (39.7% in the I/II stage, 71.4% in the III/IV stage, p = 0.029). A similar change was found in protein level. CCT7 expression differed significantly between the deep MI group (>1/2) and the superficial MI group (≤1/2) ( p = 0.039). However, there were no differences with respect to age, pathological type, and histological grade. CCT7 suppression induced a function loss in both Ishikawa and RL95-2 cells. Bioinformatics analysis demonstrated that EC patients with lower-level CCT7 expression had better overall survival ( p = 0.0081). Gene ontology enrichment indicated that “RNA binding,” “Mitochondrion,” “Translation,” and “Spliceosome” were most significantly enriched potential pathways. Five hub genes, PSMA5, PSMD14, SNRPB, SNRPG , and TXNL4 A, were all significantly upregulated in EC and had a positive correlation with CCT7 . Conclusions: CCT7 may be involved in EC development by excessively activating tumor cell function to promote MI or distant/nodal metastasis, which may contribute to the prognosis of EC patients.