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REST共抑制因子2促进子宫内膜癌的细胞增殖。

REST corepressor 2 contributes to the cell proliferation of endometrial cancer.

作者信息

Zhu Qingjuan, Yang Xin, Lv Yuchun

机构信息

N19 District Gynecology, Quanzhou First Hospital, Fujian Medical University, Quanzhou, Fujian, China.

出版信息

Front Oncol. 2025 Aug 27;15:1539263. doi: 10.3389/fonc.2025.1539263. eCollection 2025.

DOI:10.3389/fonc.2025.1539263
PMID:40936699
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12420226/
Abstract

BACKGROUND

Uterine corpus endometrial cancer (UCEC) is a prevalent gynecological malignancy. REST corepressor 2 (RCOR2), a nuclear transcription co-repressor, has been implicated in various cellular processes. However, its regulatory role in UCEC progression remains unclear.

METHODS

RCOR2 expression levels were analyzed in UCEC tissues and cell lines using qPCR, Western blotting. Functional assays, including CCK8 and colony formation assays, were used to assess the impact of RCOR2 knockdown or overexpression on UCEC cell viability and proliferation.

RESULTS

RCOR2 expression was significantly elevated in UCEC tissues compared to adjacent normal tissues. High RCOR2 expression correlated with advanced clinical stage, high histologic grade, and lymph node metastasis. ROC analysis indicated strong diagnostic value. RCOR2 expression showed a positive correlation with proliferation-related genes MKI67, CCND1, and PCNA. Functional assays revealed that RCOR2 knockdown suppressed, while overexpression promoted, proliferation of endometrial cancer cells. These effects were validated by CCK8 and colony formation assays, as well as changes in mRNA and protein levels of MKI67, CCND1, and PCNA, supporting RCOR2's role in regulating UCEC cell proliferation.

CONCLUSIONS

These findings suggest that RCOR2 promotes endometrial cancer progression by enhancing tumor cell proliferation and may serve as a potential diagnostic and therapeutic target in UCEC.

摘要

背景

子宫内膜癌（UCEC）是一种常见的妇科恶性肿瘤。REST共抑制因子2（RCOR2）是一种核转录共抑制因子，参与多种细胞过程。然而，其在UCEC进展中的调控作用仍不清楚。

方法

采用qPCR、蛋白质免疫印迹法分析UCEC组织和细胞系中RCOR2的表达水平。通过CCK8和集落形成试验等功能试验，评估RCOR2基因敲低或过表达对UCEC细胞活力和增殖的影响。

结果

与相邻正常组织相比，UCEC组织中RCOR2表达显著升高。RCOR2高表达与临床晚期、高组织学分级和淋巴结转移相关。ROC分析显示其具有较强的诊断价值。RCOR2表达与增殖相关基因MKI67、CCND1和PCNA呈正相关。功能试验表明，敲低RCOR2可抑制子宫内膜癌细胞增殖，而过表达则促进其增殖。CCK8和集落形成试验以及MKI67、CCND1和PCNA的mRNA和蛋白水平变化验证了这些作用，支持RCOR2在调节UCEC细胞增殖中的作用。

结论

这些发现表明，RCOR2通过增强肿瘤细胞增殖促进子宫内膜癌进展，可能成为UCEC潜在的诊断和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/5b0a3a7dab8c/fonc-15-1539263-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/fe5d183164f7/fonc-15-1539263-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/70e7cb52416e/fonc-15-1539263-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/22b7a1118750/fonc-15-1539263-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/d92c20407985/fonc-15-1539263-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/a66582367533/fonc-15-1539263-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/5b0a3a7dab8c/fonc-15-1539263-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/fe5d183164f7/fonc-15-1539263-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/70e7cb52416e/fonc-15-1539263-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/22b7a1118750/fonc-15-1539263-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/d92c20407985/fonc-15-1539263-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/a66582367533/fonc-15-1539263-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78eb/12420226/5b0a3a7dab8c/fonc-15-1539263-g006.jpg

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本文引用的文献

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Two GnRH-mitoxantrone Conjugates, Con-3 and Con-7, Target Endometrial Cancer Cells.两种GnRH-米托蒽醌偶联物Con-3和Con-7靶向子宫内膜癌细胞。
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