microRNA-190b (miR-190b) is abnormally expressed in multiple types of cancer, however, its role in colorectal cancer (CRC) is largely unknown. In the present study, it was demonstrated that miR-190b expression was upregulated in CRC cell lines compared with the normal epithelial colon cell line. Knockdown of miR-190b decreased proliferation, colony formation and invasion, and increased apoptosis of CRC cells. Furthermore, forkhead box protein P2 (FOXP2) was predicted as a target of miR-190b and further validated by luciferase activity reporter assay and western blotting. Rescue experiments showed that knockdown of FOXP2 reversed the inhibitory effects of miR-190b inhibitor on the behavior of the CRC cell lines. Taken together, the present study demonstrated the oncogenic role of miR-190b in CRC through regulation of FOXP2 expression.

Correlation of vitamin D with inflammatory factors, oxidative stress and T cell subsets in patients with autoimmune hepatitis were investigated. Patients with liver diseases (n=635) treated in The Sixth People's Hospital of Qingdao City from March 2015 to January 2018 were selected, among which 80 cases diagnosed with autoimmune hepatitis were included into observation group, and 80 healthy cases were included into control group. Patients with autoimmune hepatitis were further divided into normal 25-hydroxyvitamin D [25-(OH) D] group (n=40) and abnormal 25-(OH) D group (n=40) according to the level of 25-(OH) D, and divided into normal liver function group (n=40) and abnormal liver function group (n=40). 25-(OH) D, liver function, inflammatory factors, oxidative stress level and T cell subsets were compared. In the observation group, levels of 25-(OH) D, superoxide dismutase (SOD), total antioxidant capacity, and T cell subsets were lower than those in the control group (P<0.05), while levels of total bilirubin (TBIL), indirect BIL (IBIL), direct BIL (DBIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), inflammatory factors and malondialdehyde (MDA) were higher than those in the control group (P<0.05). In the normal 25-(OH) D group, levels of inflammatory factors and oxidative stress factor were lower than those in the abnormal 25-(OH) D group (P<0.05), while the SOD level, total antioxidant capacity and T cell subset counts were higher than those in the abnormal 25-(OH) D group (P<0.05). Moreover, the 25-(OH) D level in patients with autoimmune hepatitis was negatively correlated with hs-CRP, tumor necrosis factor-α (TNF-α), ALT and MDA, but positively correlated with CD3+ and CD4+ counts, SOD and total antioxidant capacity. Patients with autoimmune hepatitis, especially those with decreased level of vitamin D, are more prone to enhanced inflammatory and stress responses, decreased levels of T cell subsets and decline in immunity.

The current study mainly evaluated the plasma level of microRNA (miR)-136 in knee osteoarthritis (KOA) patients and determined if miR-136 could be used as a potential biomarker to screen KOA patients from healthy controls. It was demonstrated that plasma miR-136 was significantly decreased in the plasma of KOA patients. Moreover, the reduction in plasma miR-136 negatively correlated with the severity of KOA. Additionally, the increase in the serum interleukin (IL)-17 level positively correlated with the severity of KOA. More importantly, dual luciferase assays and western blot assays indicated that IL-17 was a target gene of miR-136. Further analysis showed that plasma miR-136 could be used as a biomarker to screen KOA patients from healthy controls. In summary, for the first time, the present study revealed that through targeting IL-17, decreased plasma miR-136 levels could be used as a potential biomarker to screen KOA patients from healthy controls.

Myocardial infarction (MI) is a heart disease with high morbidity and mortality rates, thus it is critical to identify genes that serve roles during its pathogenesis. The objective of the present study was to identify potentially relevant genes during the progression of the disease. Blood samples from patients with MI and normal controls (n=3/group) were obtained, the RNA was extracted and cDNA libraries were established. RNA sequencing (RNA-seq) was performed on a HiSeq 2500 platform and fragments per kilobase of exon per million fragments mapped was utilized to calculate the gene expression value following preprocessing of the RNA-seq data. Electronic validation of several identified differentially expressed genes (DEGs) was performed on a Gene Expression Omnibus (GEO) dataset GSE59867 (390 cases and 46 healthy controls). Functional enrichment and protein-protein interaction network analysis was conducted for DEGs. A total of 977 DEGs, including 817 upregulated and 160 downregulated genes were identified in patients with MI. These DEGs were significantly enriched for 'positive regulation of the immune system process,' 'inflammatory response,' 'regulation of I-kappaB-kinase/NF-kappaB signaling' and 'TNF signaling pathway'. A protein-protein interaction network of the top 40 DEGs was used to identify high degree genes, including interferon induced protein with tetratricopeptide repeats 3 (IFIT3), MX dynamin like GTPase 1 (MX1), major histocompatibility complex, class II, DQ α1 (HLA-DQA1), RAR related orphan receptor A (RORA), prostaglandin D2 synthase (PTGDS), cysteine rich protein 2 (CRIP2), collagen type VI α 2 chain (COL6A2) and S100 calcium binding protein P (S100P). The results of validation in the GEO dataset were consistent with the sequencing analysis. A total of eight genes, including IFIT3, MX1, HLA-DQA1, RORA, PTGDS, CRIP2, COL6A2 and S100P may therefore be considered as potentially relevant genes in the pathology of MI.