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Linc-UBC1 通过下调 p53 水平促进卵巢癌的转移和进展。

Linc-UBC1 stimulates the metastasis and progression of ovarian cancer via downregulating p53 level.

机构信息

Department of Oncology, Jiangxi Maternal and Child Health Hospital, Nanchang, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1054-1061. doi: 10.26355/eurrev_202002_20155.

DOI:10.26355/eurrev_202002_20155
PMID:32096175
Abstract

OBJECTIVE

To elucidate the role of linc-UBC1 in regulating the metastasis and progression of ovarian cancer (OC) by downregulating the p53 level.

PATIENTS AND METHODS

Relative levels of linc-UBC1 in OC tissues and paracancerous tissues were determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Differential expressions of linc-UBC1 in OC tissues with different tumor staging or tumor sizes were detected as well. Receiver operating characteristic (ROC) curves were introduced for assessing the diagnostic value of linc-UBC1 in OC. After silence of linc-UBC1, proliferative and migratory abilities of HO8910 and HEY cells were evaluated. Subcellular distribution of linc-UBC1 was analyzed. The interaction between linc-UBC1 and p53 was explored through the RNA immunoprecipitation (RIP) assay. At last, rescue experiments were conducted to uncover the role of linc-UBC1/p53 regulatory loop in influencing the progression of OC.

RESULTS

Linc-UBC1 was upregulated in OC and its level negatively correlated to that of p53. Linc-UBC1 level was higher in OC patients with advanced TNM staging or larger tumor size. Linc-UBC1 was mainly distributed in the nucleus. Silence of linc-UBC1 attenuated proliferative and migratory abilities of HO8910 and HEY cells. RIP assay verified that linc-UBC1 could inhibit the transcription of p53. Knockdown of p53 could partially reverse the regulatory effects of linc-UBC1 on regulating the progression of OC.

CONCLUSIONS

Linc-UBC1 is upregulated in OC tissues and cells. It stimulates the proliferation and metastasis of OC by downregulating p53 level, thus exerting a carcinogenic role.

摘要

目的

通过下调 p53 水平,阐明 linc-UBC1 在调节卵巢癌(OC)转移和进展中的作用。

患者和方法

通过实时定量聚合酶链反应(qRT-PCR)确定 OC 组织和癌旁组织中 linc-UBC1 的相对水平。检测 OC 组织中 linc-UBC1 的差异表达与不同肿瘤分期或肿瘤大小。引入受试者工作特征(ROC)曲线评估 linc-UBC1 在 OC 中的诊断价值。沉默 linc-UBC1 后,评估 HO8910 和 HEY 细胞的增殖和迁移能力。分析 linc-UBC1 的亚细胞分布。通过 RNA 免疫沉淀(RIP)实验探讨 linc-UBC1 和 p53 之间的相互作用。最后,进行挽救实验以揭示 linc-UBC1/p53 调节环在影响 OC 进展中的作用。

结果

linc-UBC1 在 OC 中上调,其水平与 p53 的水平呈负相关。OC 患者中 linc-UBC1 水平在 TNM 分期较晚或肿瘤较大的患者中较高。linc-UBC1 主要分布在细胞核中。沉默 linc-UBC1 可减弱 HO8910 和 HEY 细胞的增殖和迁移能力。RIP 实验验证 linc-UBC1 可抑制 p53 的转录。下调 p53 可部分逆转 linc-UBC1 对调节 OC 进展的调节作用。

结论

linc-UBC1 在 OC 组织和细胞中上调。它通过下调 p53 水平刺激 OC 的增殖和转移,从而发挥致癌作用。

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