Bioinformatics analysis of differentially expressed genes in hepatocellular carcinoma cells exposed to Swertiamarin
Bioinformatics analysis of differentially expressed genes in hepatocellular carcinoma cells exposed to Swertiamarin
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獐牙菜苷染毒肝细胞癌细胞差异表达基因的生物信息学分析
DOI：
10.7150/jca.33666
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发表时间：
2019-10
期刊：
影响因子：
--
通讯作者：
Jijun Chen
中科院分区：
文献类型：
--
作者：
Haoran Tang;Yang Ke;Zongfang Ren;Xuefen Lei;Shufeng Xiao;Tianhao Bao;Zhitian Shi;Renchao Zou;Tiangen Wu;Jian Zhou;Chang-An Geng;Lin Wang;Jijun Chen
目的：探讨苦马豆素对肝细胞癌细胞基因表达的影响。方法：观察苦参素作用于人肝癌细胞株HepG2后，细胞存活率、细胞凋亡率及侵袭力的变化。观察苦参素对SK-Hep-1细胞裸鼠移植瘤生长的影响。提取经苦马钱素处理后的HepG2细胞总RNA，用于基因芯片分析。采用生物信息学方法对基因芯片数据进行分析。结果：蛇床子素可降低人肝癌细胞株HepG2的存活率和侵袭力，增加细胞凋亡率，显著抑制SK-Hep-1裸鼠移植瘤的生长。对差异表达基因(Deg)的通路和生物学过程分析表明，PI3K-Akt是最重要的调控途径。用CGBVS和3NN分别预测了47个目标和21个目标。值得注意的是，两个程序都预测了8个靶点作为swertiamarin的靶点，其中包括两个突出的靶点Jun和STAT3。Jun和STAT3可以调节马钱素诱导的较大范围的DEGS。结论：Swertiamarin治疗导致调节细胞存活、细胞周期进展、细胞凋亡和侵袭的多种基因的表达发生显著变化。此外，这些基因中的大多数都可以聚集到PI3K、Jun、STAT3等途径网络中，这些基因是马钱子素的预测靶标。这些靶点的进一步确认将揭示苦马豆素的抗肿瘤机制，并有助于将其开发为一种新的癌症预防和治疗药物。
Aim: To explore gene expression profiling in hepatocellular carcinoma (HCC) cells exposed to swertiamarin. Methods: Cell viability, apoptosis and invasion were examined in HepG2 cells after swertiamarin treatment. Tumor growth of SK-Hep-1 cells xenografted in nude mice was monitored after swertiamarin treatment. Total RNA was isolated from HepG2 cells treated with swertiamarin for microarray analysis. The data of microarray were analyzed by bioinformatics. Results: Swertiamarin treatment decreased the viability and invasion while increased the apoptosis of HepG2 cells, and significantly inhibited the growth of SK-Hep-1 cells xenografted in nude mice. Pathway and biological process analysis of differentially expressed genes (DEGs) in swertiamarin treated HepG2 cells showed that PI3k-Akt was the most significant regulated pathway. 47 targets of swertiamarin were predicted by CGBVS while 21 targets were predicted by 3NN. Notably, 8 targets were predicted as the targets of swertiamarin by both programs, including two prominent targets JUN and STAT3. A large range of DEGs induced by swertiamarin could be regulated by JUN and STAT3. Conclusion: Swertiamarin treatment led to significant changes in the expression of a variety of genes that modulate cell survival, cell cycle progression, apoptosis, and invasion. Moreover, most of these genes can be clustered into pathway networks such as PI3K, JUN, STAT3, which are predicted targets of swertiamarin. Further confirmation of these targets will reveal the anti-tumor mechanisms of swertiamarin and facilitate the development of swertiamarin as a novel agent for cancer prevention and treatment.
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影响因子：
8.6
作者：
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影响因子：
3.6
作者：
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影响因子：
1.2
作者：
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