{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T20:07:57Z","timestamp":1788984477215,"version":"build-2803163510"},"reference-count":40,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T00:00:00Z","timestamp":1598572800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004735","name":"Natural Science Foundation of\u00a0Hunan Province","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004735","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:p><jats:bold>Objective:<\/jats:bold> 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.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> Clinical data for 87 EC cases and expression of CCT7 were analyzed. <jats:italic>CCT7<\/jats:italic> was knocked out using siRNA-<jats:italic>CCT7<\/jats:italic> 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 <jats:italic>CCT7<\/jats:italic> in EC development.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> The rates of CCT7-positive cells in EC and adjacent normal endometrium tissues had a significant difference (67.8 vs. 51.4%, <jats:italic>p<\/jats:italic> = 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, <jats:italic>p<\/jats:italic> = 0.029). A similar change was found in protein level. CCT7 expression differed significantly between the deep MI group (&amp;gt;1\/2) and the superficial MI group (\u22641\/2) (<jats:italic>p<\/jats:italic> = 0.039). However, there were no differences with respect to age, pathological type, and histological grade. <jats:italic>CCT7<\/jats:italic> suppression induced a function loss in both Ishikawa and RL95-2 cells. Bioinformatics analysis demonstrated that EC patients with lower-level <jats:italic>CCT7<\/jats:italic> expression had better overall survival (<jats:italic>p<\/jats:italic> = 0.0081). Gene ontology enrichment indicated that \u201cRNA binding,\u201d \u201cMitochondrion,\u201d \u201cTranslation,\u201d and \u201cSpliceosome\u201d were most significantly enriched potential pathways. Five hub genes, <jats:italic>PSMA5, PSMD14, SNRPB, SNRPG<\/jats:italic>, and <jats:italic>TXNL4<\/jats:italic>A, were all significantly upregulated in EC and had a positive correlation with <jats:italic>CCT7<\/jats:italic>.<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold><jats:italic>CCT7<\/jats:italic> 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.<\/jats:p>","DOI":"10.3389\/fonc.2020.01468","type":"journal-article","created":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T04:30:49Z","timestamp":1598589049000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["RETRACTED: Clinical Significance, Cellular Function, and Potential Molecular Pathways of CCT7 in Endometrial 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