Objective To summarize the progress of research about the relationship between papillary thyroid carcinoma (PTC) and Hashimoto’s thyroiditis (HT). Method The relevant literatures at home and abroad in recent years about this topic were collected and analyzed. Results Comprehensive literature reviewed, combined with the author's clinical research results, PTC and HT were indeed closely related, or there was a certain causal link. HT and PTC might both come from the same embryonic stem cells. HT was an autoimmune thyroid disease caused by abnormal immune response, and might be a triggering factor of PTC. Meanwhile, lymphocyte infiltration might play a certain protective role in anti-tumor effect. RET chromosome rearrangement, RAS point mutation and BRAF gene mutation might activate mitogen-activated protein kinase (MAPK) pathway, especially in PTC cases with HT in which RET chromosome rearrangement was more common. In the future, selective targeted therapy aiming at the activation of RET/RAS/BRAF/MAPK pathway was a promising treatment especially in advanced PTC cases. Conclusions The correlation between PTC and HT is not fully clarified. HT is a potential risk factor for PTC but the cases of PTC with HT have a better prognosis. More prospective studies will help to further clarify the correlation between two diseases.
ObjectiveTo explore the differential expressed lncRNA genes associated with formation of cholesterol gallstone, and analyze the biological functions of differential expressed lncRNA through bioinformatics.MethodsA total of 24 C57BL/6 mice were randomly divided into normal control group (n=8) and lithogenic group (n=16), which were treated with chow diets and lithogenic diets respectively for 5 weeks. After 5 weeks, mice of the lithogenic group were randomly divided into model control group (n=8) and ursodeoxycholic acid treatment group (n=8). Afterwards, mice of the normal control group were still fed with chow diets, mice of the model control group were fed with lithogenic diets, mice of the ursodeoxycholic acid treatment group were fed with ursodeoxycholic acid. After 2 weeks, collected liver tissues and gallbladder bile from the three groups, and observed gallbladder gross sample and analyzed lipids component of gallbladder bile, meanwhile detected the differential expressed lncRNA and analyzed the biological functions of differential expressed lncRNA through bioinformatics, including Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway analysis.ResultsWe successfully constructed the mice model of cholesterol gallstone. Total cholesterol level of gallbladder in the model control group had significantly higher than those of the normal control group and ursodeoxycholic acid treatment group (P<0.05), yet there was no significant difference between the normal control group and ursodeoxycholic acid treatment group (P=0.59). The levels of total bile acid, total bilirubin, and direct bilirubin had no significant difference among the three groups (P>0.05). There were 49 kinds of common overlapped difference lncRNA between the ursodeoxycholic acid treatment group and the model control group through differential expression analysis of lncRNA in liver tissues of the mice in three groups. GO and KEGG path analysis were performed separately by differential expressed lncRNA, and 88 kinds of GO terms and 18 kinds of pathways were significantly enriched from the model control group and the normal control group, 205 kinds of GO terms and 20 kinds of pathways were significantly enriched from the ursodeoxycholic acid treatment group and the normal control group.ConclusionsUrsodeoxycholic acid has therapeutic effect for cholesterol gallstone. Differential expressed lncRNAs play an important regulatory role in the formation of cholesterol gallstone and the prevention of gallstone formation by ursodeoxycholic acid treatment, which further lay the foundation in discussing specific mechanism regulated by lncRNA.