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Micronutrients in the Prevention and Improvement of the Standard Therapy for Alzheimer’s Disease
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Supplementation with vitamin D3 upregulated the expressions of miR-100 and miR-125b and reduced the growth of prostate cancer cells by decreasing their target protein E2F3, a family of transcriptional factor, responsible for proliferation and differentiation, which is highly expressed in prostate cancer cells.127 Treatment of primary cultures of human osteoblasts (HOBs) with vitamin D3 enhanced the expressions of miR-637 and miR-1228 and suppressed their target proteins type iv collagen (COL4A1) and bone morphogenic protein-2 kinase (BMP2K). Silencing the expression of miR-1228 prevented vitamin D3-induced suppression of BMP2K.128 Treatment of androgen-sensitive human prostate cancer cells (LNCaP) with vitamin D3 increased expression of miR-98 and decreased the levels of its target protein cyclin J (CCNJ) that controls mitosis, and inhibited growth of cancer cells.129 Overexpression of miR-98 reduced the growth of tumor cells, whereas silencing the expression of miR-98 abolished the anti-tumor effects of vitamin D3.129
Precision medicine in ovarian carcinoma
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
Shailendra Dwivedi, Purvi Purohit, Radhieka Misra, Jeewan Ram Vishnoi, Apul Goel, Puneet Pareek, Sanjay Khattri, Praveen Sharma, Sanjeev Misra, Kamlesh Kumar Pant
Invasive ovarian cancer tumors cover a spectrum from low-grade to high-grade malignancy, with differences in their morphologic, histologic, and clinical features. Further genomic analysis has revealed that low-grade tumors and low-malignancy potential (LMP) tumors are a separate class of tumors as compared to high-grade malignancy (HGM) tumors due to a difference in their mutated genes (high TP53, its downstream effector CDKN1A, activators of p53, such as PPM1A, and decreased levels of inhibitors of p53, UBE2D1 and ADNP in LMP tumors versus high expression of PDCD4, E2F3, MCM4, CDC20, and PCNA in HGM tumors (Bast and Mills 2010).
The urinary bladder
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
A series of genetic events has been clearly implicated in cancer formation but is outside the remit of this chapter. Activation of dominantly acting oncogenes such as ras and c-erbB-1 and -2, and transcription factors such as E2F3, have been reported in bladder cancer, as has the inactivation of tumour-suppressor genes such as p53, p21, p16 and the retinoblastoma gene. Activation of many other genes occurs including: those coding for enzymes that dissolve the basement membrane, such as the metalloproteinases (strome- lysin, collagenases and elastase), lysosomal enzymes such as the cathepsins and others including urinary plasminogen activators; angiogenic factors (e.g. vascular endothelial growth factor (VEGF]) and other peptide growth factors such as the epidermal growth factor (EGF) and its receptor (EGFR) also have a role to play, as well as the fibroblast growth factor (FGF) and its receptor-3 (FGFR-3) which was found to be altered mostly in non-muscle invasive disease. These changes are common to several tumour types, including prostate cancer. More recently, new approaches through genome-wide association studies allowed the investigation of genetic susceptibility for urothelial cancer. Several new loci were identified, but, to date, only two, NAT2 (N-acetyltransferase 2) and GSTM1 (glutathione S-transfer- ase Mu 1) have been demonstrated to be consistent germline susceptibility markers. These genetic markers do not yet have sufficient discriminatory ability to be used for clinical decision-making.
Bioinformatics analysis on differentially expressed genes of alveolar macrophage in IPF
Published in Experimental Lung Research, 2019
Huaibin Wang, Miaomiao Wang, Kun Xiao, Xu Zhang, Peng Wang, Shuyu Xiao, Huisheng Qi, Lijun Meng, Xiujun Zhang, Fuhai Shen
The 19 up-regulated DEGs were mainly enriched in pathways associated with cancer pathway. Among which, the E2F3 gene is associated with both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). The protein encoded by E2F3 is a member of the transcription factor E2F family, and the E2F family plays a vital role in controlling the cell cycle and role of tumor suppressor proteins. In the HA Al and O Nada articles, the level of E2F3 mRNA in the blood of lung cancer patients is significantly higher than that of benign lung disease or healthy people, and E2F3 mRNA is a sensitive diagnostic marker for lung cancer.20 This also shows that IPF has the same genetic variation as lung cancer, and some IPF eventually develop into lung cancer.21 KEGG enrichment analysis of downregulated DEGs showed that MAPK signal pathway was the most significant enrichment pathway. The MAPK pathway is a chain of proteins in the cell that communicates a signal from a receptor on the surface of the cell to the DNA in the nucleus of the cell.22 ERKs and JNKs in the MAPK signal pathway of fibrotic cells can significantly affect the downstream cell cycle, thereby affecting cell cycle and apoptosis.23,24 It is obvious from the PPI network diagram. The down-regulated genes related to MAPK signaling pathway were all located in the core positions of PPI network as the Figure 3, and the results were consistent with some research results.25–27 It is suggested that the down-regulation of some genes in the MAPK signaling pathway may have a significant effect on fibrosis. The combination of TNF signaling pathway and MAPK signaling pathway may affect the downstream P53 signal transduction pathway, cell cycle, and the Wnt signaling pathway, thus affecting the IPF process.
Association of Methylation Signatures at Hepatocellular Carcinoma Pathway Genes with Adiposity and Insulin Resistance Phenotypes
Published in Nutrition and Cancer, 2019
Omar Ramos-Lopez, Jose I. Riezu-Boj, Fermin I. Milagro, J. Alfredo Martinez
The E2F transcription factor 3 (E2F3) is a member of the E2F family of transcriptional factors that controls the cell cycle (40). In vitro assays found that E2F3 overexpression promoted proliferation of functional human beta cells, which could represent an important component of regenerative approaches to the treatment of T2DM (41).