八聚体转录因子1通过细胞外调节蛋白激酶/丝裂原活化蛋白激酶信号通路对胃癌细胞侵袭的影响

Octamer transcription factor 1 regulates gastric cancer invasion through mediating extracellular signal-regulated kinase/mitogen-activated protein kinases signaling pathway

目的 研究八聚体转录因子1(OCT1)对胃癌细胞侵袭能力影响,及其可能的作用机制。方法 用免疫组化法检测96例胃癌患者组织及其正常胃黏膜组织标本中OCT1的表达情况。将SGC-7901细胞分为实验组和对照组。实验组转染OCT1-siRNA质粒,对照组转染NC质粒。用蛋白质印迹法检测上皮细胞-间充质转化(EMT)和细胞外调节蛋白激酶/丝裂原活化蛋白激酶(ERK/MAPK)通路相关蛋白的表达情况,用Transwell实验法检测细胞的侵袭转移能力。结果 OCT1在癌组织和癌旁组织阳性表达率分别为62.50%(60例/96例)和3.12%(3例/96例),差异有统计学意义(P<0.001)。实验组和对照组的OCT1蛋白相对表达水平分别为0.21±0.02和0.62±0.11,MMP-2蛋白相对表达水平分别为0.19±0.01和0.71±0.13,E-cadherin蛋白相对表达水平分别为0.93±0.07和0.18±0.02,p-ERK蛋白相对表达水平分别为0.27±0.02和0.42±0.03,侵袭细胞数分别为(21.88±5.13)和(47.23±7.01)个,迁移细胞数分别为(32.55±6.23)和(89.82±9.11)个,差异均有统计学意义(均P<0.01)。结论 OCT1可通过调节细胞外调节蛋白激酶/丝裂原活化蛋白激酶信号通路的表达,进而调控胃癌细胞的迁移和侵袭能力。

Objective To study the effect of octamer transcription factor 1(OCT1) on the invasion ability of gastric cancer cells and its possible mechanism. Methods Immunohistochemical EnVinsion was used to detect the expression of OCT1 in 96 gastric cancer patient tissues and normal gastric mucosa tissue samples. The SGC-7901 cells were divided into experimental group and control group. The cells in the experimental group were transfected with OCT1-siRNA plasmid, and the cells in the control group were transfected with NC plasmid. The expression levels of epithelial-mesenchymal transition(EMT) and extracellular signal-regulated kinase/mitogen-activated protein kinases(ERK/MAPK) pathway related proteins were detect by Western Blotting. Transwell assay were used to detect the abilities of cell invasion and metastasis. Results The positive expression rates of OCT1 in cancer tissues and adjacent tissues were 62. 50%(60 cases/96 cases) and3. 12%(3 cases/96 cases) with significant difference(P< 0. 001). The relative expression levels of OCT1 protein inthe experimental and control groups were 0. 21 ± 0. 02 and 0. 62 ± 0. 11, the relative expression levels of MMP-2protein were 0. 19 ± 0. 01 and 0. 71 ± 0. 13, the relative expression levels of E-cadherin protein were 0. 93 ± 0. 07 and0. 18 ± 0. 02, the relative expression levels of p-ERK protein were 0. 27 ± 0. 02 and 0. 42 ± 0. 03, the number ofinvasive cells was(21. 88 ± 5. 13) and(47. 23 ± 7. 01), the number of migrating cells was(32. 55 ± 6. 23) and(89. 82 ± 9. 11), respectively;and the differences were statistically significant between two groups(allP< 0. 01).Conclusion OCT1 regulates the migration and invasion of gastric cancer cells through the extracellular regulatedprotein kinase/mitogen-activated protein kinase signaling pathway.