长链非编码 RNA LINP1 通过调节 PI3K/AKT 信号通路在子宫内膜癌进展中发挥癌基因作用。
Long non-coding RNA LINP1 functions as an oncogene in endometrial cancer progression by regulating the PI3K/AKT signaling pathway.
机构信息
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
出版信息
Eur Rev Med Pharmacol Sci. 2019 Aug;23(16):6830-6838. doi: 10.26355/eurrev_201908_18722.
OBJECTIVE
Endometrial cancer (EC) accounts for about 6% of new cancer cases in female and about 3% of cancer-related deaths were caused by EC. The poor prognosis is mainly due to the distant spread and poor differentiation. In the current study, we want to figure out the role of long non-coding RNA (LncRNA) LINP1 in EC progression.
PATIENTS AND METHODS
The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was involved to access the expression level of LINP1 in EC cell lines and tissues. The Cell Counting Kit-8 (CCK-8) assay, colony formation assay, transwell and Matrigel assay were recruited to figure out the ability of LINP1 in cell proliferation and metastasis in EC. Subsequently, Western blotting was used to detect the expression level of PI3K/AKT in EC. Besides, we used the tumor formation assay in vivo to examine the ability of LINP1 in tumor formation in vivo.
RESULTS
LINP1 was proved to be up-regulated in EC cell lines and tissues by qRT-PCR assay. CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that up-regulated LINP1 can facilitate cell migration and invasion. The results of Western blotting validated that LINP1 can activate PI3K/AKT signaling. Besides, the tumor formation assay verified that LINP1 can promote tumor formation in vivo.
CONCLUSIONS
Our research validated that LINP1 served as an oncogenic role in EC progression. The PI3K/AKT signaling pathway might be the underlying mechanism of EC progression. We hope our study can provide novel treatment targets and biomarkers in EC development and progression.
目的
子宫内膜癌（EC）约占女性新发癌症病例的 6%，约 3%的癌症相关死亡是由 EC 引起的。预后不良主要是由于远处转移和分化不良。在本研究中，我们想探讨长链非编码 RNA（LncRNA）LINP1 在 EC 进展中的作用。
患者和方法
采用实时定量聚合酶链反应（qRT-PCR）检测 LINP1 在 EC 细胞系和组织中的表达水平。采用细胞计数试剂盒-8（CCK-8）检测、集落形成检测、Transwell 和 Matrigel 检测评估 LINP1 在 EC 细胞增殖和转移中的作用。随后，采用 Western blot 检测 EC 中 PI3K/AKT 的表达水平。此外，我们还利用体内肿瘤形成实验检测 LINP1 在体内肿瘤形成中的作用。
结果
qRT-PCR 检测证实 LINP1 在 EC 细胞系和组织中呈上调表达。CCK-8 检测和集落形成实验表明，LINP1 过表达可促进 EC 细胞在体外的增殖。Transwell 和 Matrigel 实验结果表明，上调 LINP1 可促进细胞迁移和侵袭。Western blot 实验结果验证了 LINP1 可激活 PI3K/AKT 信号通路。此外，肿瘤形成实验验证了 LINP1 可促进体内肿瘤形成。
结论
本研究验证了 LINP1 在 EC 进展中发挥致癌作用。PI3K/AKT 信号通路可能是 EC 进展的潜在机制。我们希望本研究能为 EC 的发展和进展提供新的治疗靶点和生物标志物。
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