Interferon regulatory factor 1 (IRF1) has been found to serve as a tumor suppressor in cholangiocarcinoma, and enabled prediction of clinical progression and prognosis in our previous study. The objective of the current study is to screen and identify valuable microRNAs (miR), which target IRF1 to regulate cholangiocarcinoma cell proliferation, migration, and invasion. High expression of miR-383 was observed in cholangiocarcinoma tissues and cells. Meanwhile, we found the predicted binding site of miR-383 on the IRF1 3'-untranslated region (3'-UTR) according to the miR target database. The miR-383 expression was negatively related to IRF1 messeneger RNA (mRNA) and protein expression in cholangiocarcinoma tissue samples, and miR-383 negatively regulated IRF1 mRNA and protein expression in cholangiocarcinoma cells. Subsequently, we conducted a luciferase reporter assay to prove the predicted binding site miR-383 on IRF1 3'-UTR. Moreover, the results of the rescue study suggested that IRF1 was a functional target of miR-383 involved in regulating cholangiocarcinoma cell proliferation, migration, and invasion. Finally, we evaluated the clinical and prognostic significance of miR-383 in cholangiocarcinoma cases, and found that high expression of miR-383 was correlated with advanced tumor stage, large tumor size, present vascular invasion, and metastasis, and acted as an unfavorable independent prognostic factor. In conclusion, miR-383 serves as a tumor-suppressive miR to regulate cholangiocarcinoma cell proliferation, migration, and invasion via directly targeting IRF1.

Lung adenocarcinoma (LUAD) is one of the most prevalent malignancies. However, its mechanism and therapeutic strategy remain to be clarified. Mangiferin is a flavonoid derived from the leaves of mango trees of the lacquer family that has many pharmacological and physiological effects. This research aimed to elucidate the biological effect of mangiferin in LUAD cell lines and clarify the in vitro mechanism of mangiferin. Mangiferin was shown to significantly restrain the proliferation of LUAD cells (A549, H1299, and H2030 cells) in a dose- and time-dependent manner. Furthermore, mangiferin was capable of stimulating apoptosis, and more cells were blocked in G1 and S phase in the mangiferin-treated cells than in those not treated with mangiferin. Microarrays and micro-RNA sequencing data suggested that there is a higher level of miR-27b and miR-92a in LUAD tissues than in non-LUAD tissues. Additional experiments indicated that mangiferin may be related to the downregulated levels of miR-92a and miR-27b. In conclusion, mangiferin likely regulates proliferation and apoptosis in LUAD cells by reducing the expression levels of miR-92a and miR-27b.

Background The function of miR-31-5p in lung squamous cell carcinoma (LUSC) remains unclear, therefore, a systematic study was performed for the clinical significance and molecular mechanism of miR-31-5p in LUSC. Methods Quantitative real-time reverse transcription PCR (qRT-PCR) was utilized to test the expression level of miR-31-5p in 88 LUSC tissue samples and their matching normal tissues. Data from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) were also utilized to confirm the expression level and clinical value of miR-31-5p in LUSC. The potential target genes of miR-31-5p were predicted by several online predicted software. Gene ontology (GO), protein-protein interaction (PPI) and pathway analysis were utilized to investigate the underlying molecular mechanism of miR-31-5p in LUSC. Results The result from qRT-PCR found that there was significant difference of miR-31-5p between LUSC and normal tissues (P<0.001). Meanwhile, Data from TCGA also showed a higher expression of miR-31-5p in LUSC tissues than that in the normal tissues (P<0.001). on the basis of the data of GEO database, five GEO datasets indicated that the expression of miR-31-5p in LUSC tissues was significantly higher than that in normal lung tissues, include GSE51858 (P=0.025), GSE74190 (P<0.000), GSE16025 (P=0.031), GSE25508 (P=0.0.01), and GSE47525 (P=0.049). Moreover, in consideration of the meta-analysis, 1,012 clinical specimens were systematically analyzed via meta-analysis, clinical specimens were systematically analyzed via meta-analysis, and the results showed that the expression of miR-31-5p in LUSC was significantly higher than in the adjacent lung tissues (SMD =0, CI: 1.08–1.45, Z=13.30, P=0.000). In addition, result from GO and pathway analyses showed that potential target genes of miR-31-5p were significantly associated with 20 GO terms and 5 pathways, such as signal transduction, transmembrane receptor protein tyrosine kinase activity, plasma membrane and Rap1 signaling pathway. Meanwhile, we also found thatmiR-31-5p target genes were related to the Rap1 signaling pathway, Oxytocin signaling pathway and Proteoglycans in cancer. Furthermore, six hub genes were identified from PPI and three hub genes, including ADCY6, ADCY9 and EGFR, proved to coexist in the Rap1 signaling pathway, oxytocin signaling pathway and Melanogenesis simultaneously. Conclusions According to what has been discussed above, we speculated that miR-31-5p may play a vital role in the occurrence and development of LUSC.