SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition
SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition
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SIX1在胃癌中表达上调，通过靶向ERK通路并促进上皮-间质转化来调节增殖和侵袭
DOI：
10.1002/cbf.3361
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发表时间：
2018-10
影响因子：
3.6
通讯作者：
Mingjun Sun
中科院分区：
文献类型：
--
作者：
Ying Xie;Peng Jin;Xuren Sun;Taiwei Jiao;Yining Zhang;Yue Li;Mingjun Sun
Sine Oculis Homeobox Homoloue 1(SIX1)是一个6类同源框基因，在许多物种中都是保守的。据报道，它是一种癌基因，在许多癌症中过度表达。然而，SIX1在胃癌中的作用和调控机制尚不清楚。在我们的研究中，我们通过免疫组织化学(IHC)检测SIX1的蛋白水平，并通过CCK8和Transwell检测SIX1的增殖和侵袭效应。免疫印迹法检测细胞周期蛋白D1、MMP2、p-ERK和EMT相关蛋白的表达。我们发现SIX1在胃癌组织中有明显的高表达，并能促进胃癌细胞的增殖和侵袭。此外，SIX1过表达还增加了细胞周期蛋白D1、MMP2、p-ERK和EMT相关蛋白的表达，这些蛋白的表达均可通过下调SIX1而被抑制。综上所述，SIX1在胃癌组织中表达上调。SIX1通过靶向细胞周期蛋白D1促进胃癌细胞增殖，通过ERK信号转导促进细胞侵袭，通过靶向MMP2和E-cadherin促进EMT通路的侵袭。这些结果提示SIX1在胃癌增殖和侵袭中的潜在调控机制。
Sine oculis homeobox homologue 1 (SIX1) is a Six class homeobox gene conserved throughout many species. It has been reported to act as an oncogene and is overexpressed in many cancers. However, the function and regulatory mechanism of SIX1 in gastric cancer (GC) remains unclear. In our study, we detected protein levels of SIX1 via immunohistochemistry (IHC) and its proliferation and invasion effects via CCK8 and transwell assays. Additionally, expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins was measured by western blotting. We found that SIX1 had significantly higher expression in GC tissues and that it could promote GC cell proliferation and invasion. Also, overexpression of SIX1 increased the expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins, which could all be inhibited by knocking down SIX1. In conclusion, SIX1 is upregulated in GC tissues. It can promote GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin.Significance of the studyOur study showed that SIX1 was upregulated in GC tissues, and promoted GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin. These results suggested the potential regulatory mechanism of SIX1 in proliferation and invasion of gastric cancer.
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影响因子：
3.3
作者：
Kondratiev, Svetlana;Gnepp, Douglas R.;Laver, Nora V.
通讯作者：
Laver, Nora V.
影响因子：
--
作者：
Bae GY;Choi SJ;Lee JS;Jo J;Lee J;Kim J;Cha HJ
通讯作者：
Cha HJ
Trop2通过ERK和JNK途径诱导MMP2增强甲状腺癌的侵袭
影响因子：
3.8
作者：
Guan H;Guo Z;Liang W;Li H;Wei G;Xu L;Xiao H;Li Y
通讯作者：
Li Y
DOI：
10.1891/9780826121646.0002
发表时间：
2018-09
期刊：
Cancer Rehabilitation
影响因子：
--
作者：
K. Miller;R. Siegel;R. Khan;A. Jemal
通讯作者：
K. Miller;R. Siegel;R. Khan;A. Jemal
Six1通过上调结缔组织生长因子促进胶质母细胞瘤细胞增殖和侵袭
影响因子：
5.3
作者：
Tian Tian;Li Aimin;Lu Hong;Luo Ran;Zhang Mingzhi;Li Zhaoming
通讯作者：
Li Zhaoming