High expression of erythropoietin-producing hepatoma cell line-B2 (EphB2) predicts the efficiency of the Qingyihuaji formula treatment in pancreatic cancer CFPAC-1 cells through the EphrinB1-EphB2 pathway.
High expression of erythropoietin-producing hepatoma cell line-B2 (EphB2) predicts the efficiency of the Qingyihuaji formula treatment in pancreatic cancer CFPAC-1 cells through the EphrinB1-EphB2 pathway.
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促红细胞生成素肝癌细胞系-B2（EphB2）的高表达通过EphrinB1-EphB2途径预测清胰化积方治疗胰腺癌CFPAC-1细胞的效率
DOI：
10.3892/ol.2014.2134
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发表时间：
2014-07
期刊：
影响因子：
2.9
通讯作者：
Liu LM
中科院分区：
文献类型：
--
作者：
Hua YQ;Chen Z;Meng ZQ;Chen H;Shen JG;Wang K;Peng W;Shen YH;Liu LM
我们以前的研究表明，抑制促红细胞生成素产生的肝癌细胞系-B2（EphB 2）的表达导致促进癌症的生长，EphB 2作为胰腺癌的肿瘤抑制因子。中药清胰化积方是胰腺癌患者生存的独立保护因子，不同患者对清胰化积方的疗效不同。本研究通过观察QYHJ对不同EphB 2表达水平的细胞的抑瘤作用，探讨QYHJ对肿瘤生长抑制的作用机制。采用不同EphB 2表达水平的癌细胞建立体内皮下移植瘤模型，并给予芪愈合剂干预4周。评价肿瘤重量抑制率和肿瘤体积缩小率。流式细胞仪检测细胞周期和凋亡情况，逆转录聚合酶链反应和western blot检测mRNA和蛋白水平。结果表明，QYHJ作用后CFPAC-1、CFPAC-1对照RNAi和CFPAC-1 EphB 2 RNAi细胞的瘤重抑制率分别为31.40%、31.33%和18.36%。在CFPAC-1（P<0.05）和CFPAC-1对照RNAi（P<0.01）细胞中鉴定出统计学显著差异。此外，在CFPAC-1和CFPAC-1对照RNAi细胞中，在G 0/G1期群体中鉴定出统计学显著增加（P <0.05），并且在S期群体中鉴定出统计学显著减少（P<0.05）;然而，在QYHJ处理后的CFPAC-1 EphB 2 RNAi细胞中没有鉴定出显著差异。在表达不同水平EphB 2的细胞中，QYHJ上调Eph受体相互作用B1（EphrinB 1）的mRNA和蛋白水平，然而，QYHJ不调节EphB 2表达。在CFPAC-1和CFPAC-1对照RNAi细胞中，QYHJ处理导致细胞周期蛋白依赖性激酶6（CDK 6）mRNA（P<0.05）和蛋白质（P<0.05）水平的统计学显著降低。EphB 2的高表达预示了通过CFPAC-1细胞中EphrinB 1-EphB 2诱导的CDK 6减少抑制细胞周期的机制，对QYHJ治疗的上级响应率。因此，EphB 2作为QYHJ治疗胰腺癌CFPAC-1细胞的预测因子。
Our previous study demonstrated that inhibition of erythropoietin-producing hepatoma cell line-B2 (EphB2) expression resulted in the promotion of cancer growth, with EphB2 acting as a tumor suppressor in pancreatic cancer. Qingyihuaji formula (QYHJ), a traditional Chinese medicine, acts as an independent protective factor for pancreatic cancer patient survival and different patients have shown various responses to QYHJ treatment. In the current study, the different effects on tumor growth inhibition following QYHJ treatment in cells with different levels of EphB2 expression were investigated to reveal the mechanism. A subcutaneously transplanted tumor model using cancer cells with different levels of EphB2 expression were establishedin vivoand received a four-week QYHJ intervention. Tumor weight inhibitory rate and tumor volume deflation were evaluated. The cell cycle and apoptosis were analyzed by flow cytometry, and reverse transcription polymerase chain reaction and western blot analysis were used to assess mRNA and protein levels. The results showed that the tumor weight inhibitory rate was 31.40, 31.33 and 18.36% in CFPAC-1, CFPAC-1 control RNAi and CFPAC-1 EphB2 RNAi cells following QYHJ treatment, respectively. A statistically significant difference was identified in CFPAC-1 (P<0.05) and CFPAC-1 control RNAi (P<0.01) cells. In addition, a statistically significant increase was identified in the G0/G1 phase population (P<0.05) and a statistically significant decrease was identified in the S phase population (P<0.05) in CFPAC-1 and CFPAC-1 control RNAi cells; however, no significant difference was identified in the CFPAC-1 EphB2 RNAi cells following QYHJ treatment. QYHJ upregulated the mRNA and protein level of Eph receptor-interacting B1 (EphrinB1) in the cells that were expressing different levels of EphB2, however, QYHJ did not regulate EphB2 expression. In CFPAC-1 and CFPAC-1 control RNAi cells, the QYHJ treatment resulted in a statistically significant decrease in cyclin-dependent kinase 6 (CDK6) mRNA (P<0.05) and protein (P<0.05) levels. The high expression of EphB2 predicted the superior response rate to the QYHJ treatment through a mechanism of inhibiting the cell cycle by an EphrinB1-EphB2-induced CDK6 decrease in CFPAC-1 cells. Therefore, EphB2 acts as a predictive factor for QYHJ treatment in pancreatic cancer CFPAC-1 cells.
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影响因子：
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作者：
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通讯作者：
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DOI：
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