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HOTTIP 通过激活 PI3K/AKT 通路调控子宫内膜癌的进展。

HOTTIP regulates progression of endometrial cancer via activating PI3K/AKT pathway.

机构信息

Department of Gynecology, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Jun;22(12):3727-3733. doi: 10.26355/eurrev_201806_15252.

DOI:10.26355/eurrev_201806_15252
PMID:29949146
Abstract

OBJECTIVE

To investigate the possible role of HOTTIP in the pathogenesis of endometrial cancer (EC) and its underlying mechanism.

PATIENTS AND METHODS

76 EC tissues and 76 adjacent normal tissues were collected in this study. HOTTIP expression was detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction), and its relationship with clinical prognosis of EC patients was then analyzed. The effect of in vitro HOTTIP on proliferation, cell cycle, apoptosis, colony formation, and migration was examined, respectively. Furthermore, the impact of HOTTIP on PI3K/AKT pathway was explored.

RESULTS

HOTTIP was remarkably overexpressed in EC patients. The survival rate of EC patients with high expression of HOTTIP was lower than that of patients with low expression, whereas the pathological grade and tumor size in high expression group were markedly higher than those of low expression group. After upregulation of HOTTIP by lentivirus transfection, the proliferation, colony formation, and migration of EC cells showed a remarkable increase, whereas cell apoptosis was remarkably inhibited. In addition, high expression of HOTTIP promoted the EC development by activating PI3K/AKT pathway.

CONCLUSIONS

Overexpressed HOTTIP promotes the development of endometrial cancer via activating PI3K/AKT pathway.

摘要

目的

探讨 HOTTIP 在子宫内膜癌(EC)发病机制中的可能作用及其潜在机制。

患者与方法

本研究收集了 76 例 EC 组织和 76 例相邻正常组织。通过 qRT-PCR(定量实时聚合酶链反应)检测 HOTTIP 的表达,并分析其与 EC 患者临床预后的关系。分别检测体外 HOTTIP 对增殖、细胞周期、凋亡、集落形成和迁移的影响。此外,还探讨了 HOTTIP 对 PI3K/AKT 通路的影响。

结果

HOTTIP 在 EC 患者中显著过表达。HOTTIP 高表达的 EC 患者的生存率低于低表达的患者,而高表达组的病理分级和肿瘤大小明显高于低表达组。通过慢病毒转染上调 HOTTIP 后,EC 细胞的增殖、集落形成和迁移明显增加,而细胞凋亡明显受到抑制。此外,高表达的 HOTTIP 通过激活 PI3K/AKT 通路促进 EC 的发展。

结论

过表达的 HOTTIP 通过激活 PI3K/AKT 通路促进子宫内膜癌的发展。

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