Gene coexpression patterns can reveal gene collections with functional consistency. This study systematically constructs regulatory networks for pituitary tumours by integrating gene coexpression, transcriptional and posttranscriptional regulation. Through network analysis, we elaborate the incidence mechanism of pituitary adenoma. The Pearson’s correlation coefficient was utilized to calculate the level of gene coexpression. By comparing pituitary adenoma samples with normal samples, pituitary adenoma-specific gene coexpression patterns were identified. For pituitary adenoma-specific coexpressed genes, we integrated transcription factor (TF) and microRNA (miRNA) regulation to construct a complex regulatory network from the transcriptional and posttranscriptional perspectives. Network module analysis identified the synergistic regulation of genes by miRNAs and TFs in pituitary adenoma. We identified 142 pituitary adenoma-specific active genes, including 43 TFs and 99 target genes of TFs. Functional enrichment of these 142 genes revealed that the occurrence of pituitary adenoma induced abnormalities in intracellular metabolism and angiogenesis process. These 142 genes were also significantly enriched in adenoma pathway. Module analysis of the systematic regulatory network found that three modules contained elements that were closely related to pituitary adenoma, such as FGF2 and SP1, as well as transcription factors and miRNAs involved in the tumourigenesis. These results show that in the occurrence of pituitary adenoma, miRNA, TF and genes interact with each other. Based on gene expression, the proposed method integrates interaction information from different levels and systematically explains the occurrence of pituitary tumours. It facilitates the tracing of the origin of the disease and can provide basis for early diagnosis of complex diseases or cancer without obvious symptoms.

Temporal lobe epilepsy (TLE) is the most common epilepsy subtype with complex genetic structure. A recent study in four populations (Ireland, UK, Australia and Finland) reported an allelic association between betaine/GABA transporter-1 (𝐵𝐺𝑇-1 or 𝑆𝐿𝐶6𝐴12) and mesial temporal lobe epilepsy with hippocampal sclerosis. To demonstrate the association between 𝑆𝐿𝐶6𝐴12 gene polymorphisms and TLE, TaqMan method was used to genotype five single-nucleotide polymorphisms of 𝑆𝐿𝐶6𝐴12 gene in 358 TLE patients and 596 nonepileptic control subjects of Chinese Han origin. Real-time PCR was used to detect the effects of variations on gene expression associated with TLE. Though, the single-marker analysis did not demonstrate allelic association with TLE, rs542736–rs557881 interaction showed significant association. The 𝑆𝐿𝐶6𝐴12 expression levels in peripheral blood mononuclear cells were significantly higher in TLE patients than in control subjects and were correlated to rs542736 G–rs557881 A haplotypes. Our preliminary results suggested combined effect of two common polymorphisms on SLC6A12 gene may be associated with TLE, but the precise mechanism needs further investigation.