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LINC00963 通过激活 PI3K/AKT 通路促进肝癌进展。

LINC00963 promotes hepatocellular carcinoma progression by activating PI3K/AKT pathway.

机构信息

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepato-Pancreato-Biliary Surgery, Peking University Cancer Hospital anad Institute, Beijing, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Mar;22(6):1645-1652. doi: 10.26355/eurrev_201803_14574.

DOI:10.26355/eurrev_201803_14574
PMID:29630107
Abstract

OBJECTIVE

To explore the role of LINC00963 in the pathogenesis of hepatocellular carcinoma and its underlying mechanisms.

PATIENTS AND METHODS

The expression level of LINC00963 in 48 cases of hepatocellular carcinoma (HCC) tissues and paracancerous tissues were detected by quantitative Real-time (qRT-PCR). Survival analysis was carried out based on the expression level of LINC00963. The association between the expression level of LINC00963 and clinical characteristics of these subjects was analyzed by x2-test. The proliferation and cell cycle of HCC cells after transfection of LINC00963 overexpression plasmids were evaluated by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively.

RESULTS

The expression level of LINC00963 in HCC tissues was remarkably higher than that in paracancerous tissues, indicating a potential diagnostic significance of LINC00963. The progression-free -with the tumor size and TNM stage, but not with age, gender, histological type and lymph node metastasis. Overexpression of LINC00963 significantly enhanced the proliferation ability of HepG2 and HCC cells and prolonged their G0/G1 phase. Furthermore, the PI3K/AKT expression was increased after overexpression of LINC00963, while AKT siRNA effectively reversed the prolonged G0/G1 phase caused by LINC00963 overexpression.

CONCLUSIONS

Our data revealed that LINC00963 was upregulated in HCC, which significantly extended the G0/G1 phase of HCC cells by activating PI3K/AKT pathway and promoting the proliferative ability of HCC cells. LINC00963 may be involved in the HCC development.

摘要

目的

探讨长链非编码 RNA LINC00963 在肝细胞癌发病机制中的作用及其潜在机制。

方法

采用实时荧光定量 PCR(qRT-PCR)检测 48 例肝癌(HCC)组织及癌旁组织中 LINC00963 的表达水平,基于 LINC00963 的表达水平进行生存分析。采用卡方检验分析 LINC00963 的表达水平与受试者临床特征的相关性。通过细胞计数试剂盒-8(CCK-8)检测和流式细胞术分别评估转染 LINC00963 过表达质粒后 HCC 细胞的增殖和细胞周期。

结果

LINC00963 在 HCC 组织中的表达水平明显高于癌旁组织,提示 LINC00963 具有潜在的诊断意义。LINC00963 的表达水平与肿瘤大小和 TNM 分期相关,与年龄、性别、组织学类型和淋巴结转移无关。过表达 LINC00963 显著增强了 HepG2 和 HCC 细胞的增殖能力,并延长了它们的 G0/G1 期。此外,过表达 LINC00963 后 PI3K/AKT 的表达增加,而 AKT siRNA 有效逆转了 LINC00963 过表达引起的 G0/G1 期延长。

结论

我们的数据表明,LINC00963 在 HCC 中上调,通过激活 PI3K/AKT 通路延长 HCC 细胞的 G0/G1 期,并促进 HCC 细胞的增殖能力。LINC00963 可能参与 HCC 的发生发展。

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