Biomimetic ZIF-8 Nanoparticles: A Novel Approach for Biomimetic Drug Delivery Systems.

Metal-organic frameworks (MOFs) are porous materials resulting from the coordination of metal clusters or ions with organic ligands, merging macromolecular and coordination chemistry features. Among these, zeolitic imidazolate framework-8 (ZIF-8) stands out as a widely utilized MOF known for its robust stability in aqueous environments owing to the robust interaction between its constituent zinc ions (Zn) and 2-methylimidazole (2-MIM). ZIF-8 readily decomposes under acidic conditions, serving as a promising candidate for pH-responsive drug delivery systems.

YAP prevents senescence of dermal fibroblast and inhibits melanogenesis via paracrine effect of DKK1.

Senile skin hyperpigmentation displays remarkable histopathological features of dermal aging. The crosstalk between melanocytes and dermal fibroblasts plays crucial roles in aging-related pigmentation. While senescent fibroblasts can upregulate pro-melanogenic factors, the role of anti-melanogenic factors, such as dickkopf1 (DKK1), and the upstream regulatory mechanism during aging remain obscure.

Jun/Fos promotes migration and invasion of hepatocellular carcinoma cells by enhancing BORIS promoter activity.

The Brother of the Regulator of Imprinted Sites (BORIS), as a specific indicator of hepatocellular carcinoma, exhibits a significant increase in expression. However, its upstream regulatory network remains enigmatic. Previous research has indicated a strong correlation between the Hippo pathway and the progression of hepatocellular carcinoma.

BORIS variant SF2(C2/A4) promotes the malignant development of liver cancer by activating epithelial-mesenchymal transition and hepatic stellate cells.

The underlying mechanisms of metastasis and recurrence of liver cancer remain largely unknown. Here, we found that Brother of the Regulator of Imprinted Sites (BORIS) variant SF2(C2/A4) was highly expressed in high metastatic potential hepatocellular carcinoma (HCC) cells and clinical tumor samples, related to the formation of satellite nodules. Its over expression promoted self-renewal, the expression of tumor stem cell markers, chemoresistance, wound healing rate, invasion and metastasis of HepG2 and Hep3B cells; reinforced epithelial-mesenchymal transition (EMT), decreased the expression of E-cadherin and increased N-cadherin and Vimentin.

AMPKα2/HNF4A/BORIS/GLUT4 pathway promotes hepatocellular carcinoma cell invasion and metastasis in low glucose microenviroment.

Increasing evidence has revealed that the invasion and metastasis of HCC are intimately related to the low-glucose microenvironment, but the intrinsic regulatory mechanism remains unclear. It has been well documented that AMPK regulates the transcriptional expression of GLUT4 and its catalytic subunit AMPKα2 can negatively regulate the downstream target molecule HNF4A. Meanwhile, BORIS (Brother of the Regulator of Imprinted Sites) is able to modulate the Warburg effect by regulating the splicing of pyruvate kinase M2 (PKM2), a critical enzyme in glycolysis.

Establishment and evaluation of cell and animal models expressing BORIS subfamily 2 variant.

Background: The possibility of a cancer vaccine aimed at stimulating or mobilizing the body's immune system to control and kill tumor cells is emerging as a potential new strategy for tumor immunological therapy. CCCTC-binding Factor Like (CTCFL)/Brother of the Regulator of Imprinted Sites (BORIS), a cancer-testis antigen (CTA), has 23 mRNA splice variants classified into six subfamilies (sfs) and potentially encodes 17 distinct polypeptides. Based on our previous long-term research on hepatocellular carcinoma (HCC), we were particularly interested in whether BORIS sf2 could be a promising candidate for immunotherapy targeting liver cancer cells.