Communication between nonalcoholic fatty liver disease and atherosclerosis: Focusing on exosomes.

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic hepatic disorder on a global scale. Atherosclerosis (AS), a leading cause of cardiovascular diseases, stands as the primary contributor to mortality among patients diagnosed with NAFLD. However, the precise etiology by which NAFLD causes AS remains unclear. Exosomes are nanoscale extracellular vesicles secreted by cells, and are considered to participate in complex biological processes by promoting cell-to-cell and organ-to-organ communications. As vesicles containing protein, mRNA, non-coding RNA and other bioactive molecules, exosomes can participate in the development of NAFLD and AS respectively. Recently, studies have shown that NAFLD can also promote the development of AS via secreting exosomes. Herein, we summarized the recent advantages of exosomes in the pathogenesis of NAFLD and AS, and highlighted the role of exosomes in mediating the information exchange between NAFLD and AS. Further, we discussed how exosomes play a prominent role in enabling information exchange among diverse organs, delving into a novel avenue for investigating the link between diseases and their associated complications. The future directions and emerging challenges are also listed regarding the exosome-based therapeutic strategies for AS under NAFLD conditions.

Systematic analysis of the role of SLC52A2 in multiple human cancers.

BACKGROUND: In humans, riboflavin must be obtained through intestinal absorption because it cannot be synthesized by the body. SLC52A2 encodes a membrane protein belonging to the riboflavin transporter protein family and is associated with a variety of diseases. Here, we systematically explore its relevance to multiple human tumors. METHODS: We analyzed the association of SLC52A2 with 33 tumors using publicly available databases such as TCGA and GEO. We verified the SLC52A2 expression in hepatocellular carcinoma, gastric cancer, colon cancer, and rectal cancer using immunohistochemistry. RESULTS: We report that SLC52A2 was highly expressed in almost all tumors, and the immunohistochemical results in the hepatocellular, gastric, colon, and rectal cancers were consistent with the above. SLC52A2 expression was linked to patient overall survival, disease-specific survival, progression-free interval, diagnosis, mutations, tumor mutational burden, microsatellite instability, common immune checkpoint genes, and immune cells infiltration. Enrichment analysis showed that SLC52A2 was mainly enriched in oocyte meiosis, eukaryotic ribosome biogenesis, and cell cycle. In hepatocellular carcinoma, the SLC52A2 expression is an independent prognostic factor. The SNHG3 and THUMPD3-AS1/hsa-miR-139-5p-SLC52A2 axis were identified as potential regulatory pathways in hepatocellular carcinoma. CONCLUSION: In conclusion, we have systematically described for the first time that SLC52A2 is closely associated with a variety of tumors, especially hepatocellular carcinoma.

Effect of high WDR5 expression on the hepatocellular carcinoma prognosis.

WD repeat domain 5 (WDR5) serves an important role in various biological functions through the epigenetic regulation of gene transcription. Aberrant expression of WDR5 has been observed in various types of human cancer, including prostate cancer, breast cancer and leukemia. However, the role of WDR5 expression and its clinical implications in hepatocellular carcinoma (HCC) remain largely unknown. The present study investigated the WDR5 expression pattern in HCC. It was demonstrated that the mRNA and protein levels of WDR5 were upregulated in HCC cancer tissues compared with normal adjacent tissues using reverse transcription-quantitative polymerase chain reaction and western blotting. Furthermore, the elevated WDR5 protein level was significantly associated with the histological grade (P=0.038), tumor size (P=0.023), tumor-node-metastasis stage (P=0.035) and reduced long-term survival time. Additionally, it was demonstrated through the shRNA-mediated knockdown of WDR5 in HCC cells in vitro that WDR5 expression promotes cell proliferation using an MTT assay. Taken together, the results suggested that WDR5 overexpression may have an oncogenic effect in HCC, and may be a promising biomarker for the diagnosis and prognosis of HCC.