Search

Thyroid cancer is a frequent endocrine cancer, and its incidence continues to rise globally. MEX3A has been revealed to be strongly expressed in many human malignant tumors including thyroid cancer and is related to patients’ prognosis. However, the molecular mechanisms underlying the tumorigenic capacities of MEX3A in thyroid cancer have not been elucidated. In this study, we verified that MEX3A is overexpressed in thyroid cancer tissues and cell lines. High levels of MEX3A positively link to AJCC stage. Moreover, MEX3A depletion attenuated abilities of proliferation and migration, ameliorated cell apoptosis as well as arrested tumor growth. Mechanistically, we found that the tumor-promoting effects of MEX3A in thyroid cancer was mediated by CREB1. Silencing CREB1 could relieve the promotion of MEX3A elevation on malignant phenotypes of thyroid cancer cells. Together, the results of this study highlight the importance of the MEX3A-CREB1 interaction for thyroid cancer cells to growth and suggest the potential of MEX3A as a therapeutic target for thyroid cancer.

Objective: A few former studies suggested there are partial overlaps in abnormal brain structure and cognitive function between Hypochondriasis (HS) and schizophrenia (SZ). But their differences in brain activity and cognitive function were unclear. Methods: 21 HS patients, 23 SZ patients, and 24 healthy controls (HC) underwent Resting-state functional magnetic resonance imaging (rs-fMRI) with the regional homogeneity analysis (ReHo), subsequently exploring the relationship between ReHo value and cognitive functions. The support vector machines (SVM) were used on effectiveness evaluation of ReHo for differentiating HS from SZ. Results: Compared with HC, HS showed significantly increased ReHo values in right middle temporal gyrus (MTG), left inferior parietal lobe (IPL) and right fusiform gyrus (FG), while SZ showed increased ReHo in left insula, decreased ReHo values in right paracentral lobule. Additionally, HS showed significantly higher ReHo values in FG, MTG and left paracentral lobule but lower in insula than SZ. The higher ReHo values in insula were associated with worse performance in MCCB in HS group. SVM analysis showed a combination of the ReHo values in insula and FG was able to satisfactorily distinguish the HS and SZ patients. Conclusion: our results suggested the altered default mode network (DMN), of which abnormal spontaneous neural activity occurs in multiple brain regions, might play a key role in the pathogenesis of HS, and the resting-state alterations of insula closely related to cognitive dysfunction in HS. Furthermore, the combination of the ReHo in FG and insula was a relatively ideal indicator to distinguish HS from SZ.

This study aimed to investigate the alterations of causal connectivity between the brain regions in Adolescent-onset schizophrenia (AOS) patients. Thirty-two first-episode drug-naïve AOS patients and 27 healthy controls (HC) were recruited for resting-state functional MRI scanning. The brain region with the between-group difference in regional homogeneity (ReHo) values was chosen as a seed to perform the Granger causality analysis (GCA) and further detect the alterations of causal connectivity in AOS. AOS patients exhibited increased ReHo values in left superior temporal gyrus (STG) compared with HCs. Significantly decreased values of outgoing Granger causality from left STG to right superior frontal gyrus and right angular gyrus were observed in GC mapping for AOS. Significantly stronger causal outflow from left STG to right insula and stronger causal inflow from right middle occipital gyrus (MOG) to left STG were also observed in AOS patients. Based on assessments of the two strengthened causal connectivity of the left STG with insula and MOG, a discriminant model could identify all patients from controls with 94.9% accuracy. This study indicated that alterations of directional connections in left STG may play an important role in the pathogenesis of AOS and serve as potential biomarkers for the disease.

Trefoil factor 1 (TFF1) is a tumor suppressor gene that encodes a peptide belonging to the trefoil factor family of protease‑resistant peptides. Although TFF1 expression is frequently lost in gastric carcinomas (GCs), the tumorigenic pathways that are affected have yet to be determined. The aim of the current study was to identify the mechanism(s) by which the TFF1 gene is regulated in gastric carcinogenesis. In this study, TFF1 was shown to be silenced or downregulated in gastric tumor tissue compared with matched non‑cancerous tissue. In addition, human gastric cells weakly expressed TFF1. The hypermethylation status in the promoter CpG islands appeared to be correlated with TFF1 expression levels in gastric cell lines or specimen tissue. Further molecular analysis indicated that the CpG islands play a role in the promoter activity of the TFF1 gene. The expression of TFF1 and DNA methylation of its promoter affected cell proliferation and apoptosis. The expression of TFF1 in gastric cell lines was restored with a demethylating agent, 5‑azacytidine. Low expression of TFF1 in gastric cell lines and cancer tissue is associated with TP 53. In conclusion, the current study demonstrates that DNA methylation is a key mechanism of silencing TFF1 expression in human gastric cells and TFF1 gene hypermethylation of the CpG islands is a potential biomarker for GC.