AUTHOR=Wang Liwen , Zhou Wei , Li Hui , Yang Hui , Shan Nianchun 

TITLE=RETRACTED: Clinical Significance, Cellular Function, and Potential Molecular Pathways of CCT7 in Endometrial Cancer

JOURNAL=Frontiers in Oncology

VOLUME=10

YEAR=2020

URL=https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2020.01468

DOI=10.3389/fonc.2020.01468

ISSN=2234-943X

ABSTRACT=<p><bold>Objective:</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.</p><p><bold>Methods:</bold> Clinical data for 87 EC cases and expression of CCT7 were analyzed. <italic>CCT7</italic> was knocked out using siRNA-<italic>CCT7</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 <italic>CCT7</italic> in EC development.</p><p><bold>Results:</bold> The rates of CCT7-positive cells in EC and adjacent normal endometrium tissues had a significant difference (67.8 vs. 51.4%, <italic>p</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, <italic>p</italic> = 0.029). A similar change was found in protein level. CCT7 expression differed significantly between the deep MI group (&gt;1/2) and the superficial MI group (≤1/2) (<italic>p</italic> = 0.039). However, there were no differences with respect to age, pathological type, and histological grade. <italic>CCT7</italic> suppression induced a function loss in both Ishikawa and RL95-2 cells. Bioinformatics analysis demonstrated that EC patients with lower-level <italic>CCT7</italic> expression had better overall survival (<italic>p</italic> = 0.0081). Gene ontology enrichment indicated that “RNA binding,” “Mitochondrion,” “Translation,” and “Spliceosome” were most significantly enriched potential pathways. Five hub genes, <italic>PSMA5, PSMD14, SNRPB, SNRPG</italic>, and <italic>TXNL4</italic>A, were all significantly upregulated in EC and had a positive correlation with <italic>CCT7</italic>.</p><p><bold>Conclusions:</bold><italic>CCT7</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.</p>