Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.

Cancer can be induced by a variety of possible causes, including tumor suppressor gene failure and proto-oncogene hyperactivation. Tumor-associated extrachromosomal circular DNA has been proposed to endanger human health and speed up the progression of cancer. The amplification of ecDNA has raised the oncogene copy number in numerous malignancies according to whole-genome sequencing on distinct cancer types. The unusual structure and function of ecDNA, and its potential role in understanding current cancer genome maps, make it a hotspot to study tumor pathogenesis and evolution. The discovery of the basic mechanisms of ecDNA in the emergence and growth of malignancies could lead researchers to develop new cancer therapies. Despite recent progress, different aspects of ecDNA require more investigation. We focused on the features, and analyzed the bio-genesis, and origin of ecDNA in this review, as well as its functions in neuroblastoma and glioma cancers.

Comparative analysis of protein-protein interaction networks in metastatic breast cancer.

Metastatic lesions leading causes of the majority of deaths in patients with the breast cancer. The present study aimed to provide a comprehensive analysis of the differentially expressed genes (DEGs) in the brain (MDA-MB-231 BrM2) and lung (MDA-MB-231 LM2) metastatic cell lines obtained from breast cancer patients compared with those who have primary breast cancer. We identified 981 and 662 DEGs for brain and lung metastasis, respectively. Protein-protein interaction (PPI) analysis revealed seven shared (PLCB1, FPR1, FPR2, CX3CL1, GABBR2, GPR37, and CXCR4) hub genes between brain and lung metastasis in breast cancer. Moreover, GNG2 and CXCL8, C3, and PTPN6 in the brain and SAA1 and CCR5 in lung metastasis were found as unique hub genes. Besides, five co-regulation of clusters via seven important co-expression genes (COL1A2, LUM, SPARC, THBS2, IL1B, CXCL8, THY1) were identified in the brain PPI network. Clusters screening followed by biological process (BP) function and pathway enrichment analysis for both metastatic cell lines showed that complement receptor signalling, acetylcholine receptor signalling, and gastric acid secretion pathways were common between these metastases, whereas other pathways were site-specific. According to our findings, there are a set of genes and functional pathways that mark and mediate breast cancer metastasis to the brain and lungs, which may enable us understand the molecular basis of breast cancer development in a deeper levele to the brain and lungs, which may help us gain a more complete understanding of the molecular underpinnings of breast cancer development.