MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targeting MAPK1.
MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targeting MAPK1.
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DOI：
10.18632/oncotarget.21037
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发表时间：
2017-10-13
期刊：
影响因子：
--
通讯作者：
Guo R
中科院分区：
文献类型：
--
作者：
Chang L;Zhang D;Shi H;Bian Y;Guo R
子宫内膜癌（EC）是世界上最常见的妇科恶性肿瘤之一，发病率超过7%。其发病机制至今尚未明确阐明，这对EC治疗至关重要。本研究的目的是研究miR-143与丝裂原激活蛋白激酶1（MAPK1）之间的靶关系，并探讨miR-143通过靶向MAPK1对子宫内膜癌（EC）细胞的影响。我们收集 EC 组织和邻近组织，并用 lipofectamine 将 miR-143 模拟物和 MAPK1 siRNA 转染到 EC 细胞中。采用逆转录聚合酶链反应（RT-PCR）和蛋白质印迹法检测miR-143和MAPK1 mRNA的表达以及MAPK1蛋白的表达。应用细胞计数试剂盒8、伤口愈合实验、流式细胞仪和Transwell实验检测EC细胞增殖、迁移、细胞周期和侵袭能力的变化。我们通过生物信息学分析预测了miR-143的靶基因。发现 MiR-143 在 EC 组织和细胞中表达不足。在人EC细胞系HEC-1B中过表达miR-143或敲低MAPK1可抑制EC细胞增殖、迁移和侵袭并诱导细胞凋亡。 MAPK1被证实是miR-143的靶基因。 miR-143过表达可以有效抑制HEC-1B细胞中MAPK1 mRNA和蛋白的表达。总的来说，miR-143可能抑制EC细胞的增殖、迁移和侵袭，并通过抑制MAPK1促进EC细胞凋亡。这些发现为EC的临床治疗提供了新的和潜在的治疗方法。
Endometrial cancer (EC) is one of the most commonly diagnosed gynecologic malignancies in the world, with the morbidity rate of over 7%. The mechanism of the pathogenesis has not been specifically elucidated to date, which is imperative for EC treatment. The aim of our study was to investigate the target relationship between miR-143 and mitogen-activated protein kinase 1 (MAPK1) and explore the effect of miR-143 on the endometrial cancers (EC) cells through targeting MAPK1. We collected EC tissues and adjacent tissues, and transfected miR-143 mimics and MAPK1 siRNA into EC cells with lipofectamine. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot were used to examine the expression of miR-143 and MAPK1 mRNA and the protein expression of MAPK1. Cell counting kit-8, wound healing assay, flow cytometry and transwell assay were applied to examining the alteration of the proliferation, migration, cell cycle and invasion ability of EC cells. We predicted the targeting gene of miR-143 through bioinformatics analysis. MiR-143 was found under-expressed in EC tissues and cells. Overexpression of miR-143 or knockdown of MAPK1 in human EC cell line HEC-1B inhibited the EC cell proliferation, migration and invasion and induced apoptosis. MAPK1 was verified to be a target gene of miR-143. MiR-143 overexpression could effectively inhibit mRNA and protein expression of MAPK1 in HEC-1B cells. Collectively, miR-143 might inhibit the proliferation, migration and invasion of EC cells, and promote the apoptosis of EC cells by suppressing MAPK1. These findings provided a view for new and potential therapeutic method for the clinical treatment of EC.
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影响因子：
5.2
作者：
Bruchim I;Sarfstein R;Werner H
通讯作者：
Werner H
DOI：
10.1016/j.bbrc.2016.01.066
发表时间：
2016-02-05
影响因子：
3.1
作者：
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通讯作者：
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影响因子：
2.9
作者：
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通讯作者：
Zhou H
影响因子：
--
作者：
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通讯作者：
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影响因子：
9.7
作者：
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通讯作者：
Cha, Hyuk-Jin