Interpreting the MicroRNA-15/107 family: interaction identification by combining network based and experiment supported approach
Interpreting the MicroRNA-15/107 family: interaction identification by combining network based and experiment supported approach
复制标题
解读 MicroRNA-15/107 家族:结合基于网络和实验支持的方法进行相互作用识别
DOI:
10.1186/s12881-019-0824-9
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发表时间:
2019
影响因子:
--
通讯作者:
Lu Shemin
中科院分区:
文献类型:
--
作者:
Wang Si;Zhu Wenhua;Xu Jing;Guo Yuanxu;Yan Jidong;Meng Liesu;Jiang Congshan;Lu Shemin
BackgroundThe highly conservative miR-15/107 family (also named as miR-15/107 gene group) including ten miRNA members is currently recognized strongly implicated in multiple human disorders. Some studies focus on the entire family rather than individual miRNA for a bigger picture, while there is also certain signature dysregulation for some of the individual miRNA implicated even in the same disorder.MethodsFaced with the exponential growth of experimental evidence, our study tries to analyze their function and target interactions using various bioinformatics tools.ResultsFirstly, the evolutionary conservative “AGCAGC” sequence and possible clustered transcriptional pattern were described. Secondly, both the experimentally validated and bioinformatically predicted miRNA-target gene relationship of the entire family was analyzed to understand the mechanism of underlying collective effects for target regulation from the miR-15/107 family. Moreover, pathway analysis among miR-15/107 family was performed and displayed in detail, while its impact on cell proliferation is experimentally validated. Eventually, the dysregulation of miR-15/107 in diseases was discussed.ConclusionsIn summary, our study proposes that the collective functions and implication of miR-15/107 family in various human diseases are achieved relying on the massive overlapping target genes. While the minor differences within target gene interaction among family members could also explain the signature behavior for some of the individual miRNA in aspects such as its disease-specific dysregulation and various participation in pathways.