[Research progress on the relationship between dietary patterns and metabolic-associated fatty liver disease].

Globally, metabolic-asssociated fatty liver disease has become a significant health burden due to its complex pathogenesis, and there are no specific and effective therapeutic drugs to date. The onset and progression of metabolic-asssociated fatty liver disease is closely associated with improper dietary habits. The cornerstone to treat metabolic-asssociated fatty liver disease is weight loss through a well-balanced diet. This article summarizes and discusses the research progress at home and abroad in relationship to metabolic-asssociated fatty liver disease and dietary patterns such as the Mediterranean diet, the DASH diet, an energy-restricted balanced diet, a low fat diet, a low carbohydrate diet, a western diet, an animal food diet, a traditional diet, and others. In addition, it categorizes the effects of various dietary patterns on the prevention, treatment, or induction of several issues that need further metabolic-asssociated fatty liver disease research for subsequent reference.

LncRNA TSLNC8 inhibits proliferation of breast cancer cell through the miR-214-3p/FOXP2 axis.

OBJECTIVE: In multiple cancers, heterozygosity is frequently lost for the tumor-suppressive long noncoding RNA (lncRNA). The expression, function, and molecular mechanisms of tumor suppressive lncRNA on chromosome 8p12 (TSLNC8) in breast cancer are still unknown. MATERIALS AND METHODS: QRT-PCR assays were carried out to evaluate the level of TSLNC8 in breast cancer tissues and cell lines. MTT, colony formation, and anchorage-independent growth assays were performed to investigate the effect of TSLNC8 on cell proliferation, and flow cytometry assays were conducted to detect cell percent of different phases. Luciferase reporter assays were used to confirm the interaction of different molecules. RESULTS: TSLNC8 is significantly increased in breast cancer tissues and cell lines. Up-regulation of TSLNC8 reduces the proliferation capacity of breast cancer cells and the transition from G1 to S phase of the cell cycle. Further analysis indicated that TSLNC8 could directly bind to miR-214-3p. Up-regulation of miR-214-3p may attenuate the suppressive role of TSLNC8 on the proliferation capacity of breast cancer cells. Moreover, miR-214-3p was found to directly interact with the 3'-untranslated region (UTR) of Forkhead box P2 (FOXP2) in luciferase assays, suggesting that FOXP2 may be one of the downstream targets of miR-412-3p. CONCLUSIONS: TSLNC8 was found to inhibit the proliferation and G1/S phase transition of breast cancer cells, an effect mediated by miR-214-3p/FOXP2 axis. Our study provides evidence that TSLNC8 may act as a suppressive lncRNA and represent a novel therapeutic target for breast cancer therapy.