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Nuclear Receptor Coactivators: Mechanism and Therapeutic Targeting in Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Andrew Cannon, Christopher Thompson, Rakesh Bhatia, Sushil Kumar
Expression of NCOA2 in CRC has been investigated in a study [31], which identified a fusion transcript between LACTB2 and NCOA2 from CRC-patient tumor samples, which was absent in normal colonocytes. Albeit its expression was detected in only six of 99 tumor samples with no expression in adjacent normal samples. The study by Yu et al. demonstrate by RT-PCR and IHC that NCOA2 expression is downregulated in CRC tumors compared to normal colon tissue and its CRC-specific actions, in contrast to many other malignancies, is tumor suppressive. The group was able to demonstrate using two minimal NCOA2-expressing CRC cell lines, HCT116 and SW1116, that transfection of NCOA2 was able to abrogate colony formations, induce apoptosis, and reduce both migration and invasion of cancer cells. Additionally, overexpressing NCOA2 substantially reduced the volume and weight of murine flank xenograft tumors. Given that NCOA2-mediated transcription increases Frzb, a regulator of the Wnt/β-catenin pathway, Yu and colleagues proposed that NCOA2 downregulation in CRC cells might facilitate increased Wnt signaling, and Wnt-luciferase assay confirmed that NCOA2 transfection reduced β-catenin translational activity. Gene microarray further confirmed that NCOA2 transfection resulted in a 3-fold or greater reduction in 38% of Wnt-associated genes compared to vector-only transfected cells. Notably, this study overlooked the need to correlate NCOA2 expression in CRC-patients to disease characteristics such as progression rates or overall survival.
Proteome Changes Associated with the VEGFR Pathway and Immune System in Diabetic Macular Edema Patients at Different Diabetic Retinopathy Stages
Published in Current Eye Research, 2022
Ruyi Han, Ruowen Gong, Wei Liu, Gezhi Xu
The biological processes associated with the DEPs in Group A included proteolysis, negative regulation of cell proliferation, cytoskeleton organization, microtubule-based processes, extracellular matrix organization, regulation of the immune response, and complement activation (Figure 2(A)). Proteins involved in the negative regulation of cell proliferation included CDKN2C, FRZB, HGS, FTH1, DDX20, and TNS2. Proteins associated with extracellular matrix organization included FBN2, COL3A1, LAMA2, ITGA2B, and ICAM1. Proteins associated with the immune response and complement activation included COL3A1, ICAM1, IGHV2-5, IGKV3D-11, IGKV1D-12, and C1QC.