Lignant lung tissues is shown in PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26240184 Table 1. The mRNA levels of the 16 genes in the lung cancer tissues were Vorapaxar site compared with those in the adjacent nonmalignant lung tissues using the paired t-test. The two genes selected from the RSL were significantly down-regulated in the tumor tissuesWu et al. BMC Cancer 2013, 13:44 http://www.biomedcentral.com/1471-2407/13/Page 5 ofas compared with the adjacent nonmalignant lung tissues (GPX3, P = 0.000 and TIMP3, P = 0.000), and six genes selected from the FSL were significantly up-regulated in the lung cancer tissues (DDR1, P = 0.009; HSP90B1, P = 0.000; SDC1, P = 0.007; RPSA, P = 0.013; ERGIC3, P = 0.000; and LPCAT1 P = 0.036). However, seven genes selected from FSL (FOXA2, C4BPA, SCGB3A1, DDX58, CCNDBP, TMSB4X, and CXCL17), and one gene selected from both FSL as well as RSL (CD9), were up-regulated in the lung cancer tissues, but not significantly (P > 0.05). The tendency of the seven genes expressions was consistent with that of the FSL which represented genes up-regulated in cancer tissues. We noted that CD9, present in both the FSL and RSL, was increased in 41.2 of lung cancer cases.Perhaps the presence of CD9 in the RSL was a false signal. Over-expression of two genes (ERGIC3 and LPCAT1) had not been previously linked to lung cancer. We opted to focus on ERGIC3 in this study.Expression of ERGIC3 mRNA in cultured cellsSimilar to the results we found in lung cancer tissues, in the lung cancer cell lines, the mRNA levels of ERGIC3 showed up to 44.9- (in SPCA-1), 61.4- (in EPLC-32M1), 60.8- (in GLC-82), 22.1- (in NCI-H446), 16.0- (in A549), 32.1- (in 801D) fold increase, compared to the immortalized normal bronchial epithelial cells, BEAS-2B.Table 1 Altered expression of the 16 genes in lung cancer tissues compared with their adjacent nonmalignant lung tissues using quantitative RT-PCR (q-RT-PCR)Gene GPX3 TIMP3 Library RSL RSL Percentage 85 (29/34)# 85 (29/34) Main Functions Detoxification of hydrogen peroxide. Suppresses prostate cancer growth and metastasis. Degradation of the extracellular matrix. A mediator for checking inflammation. Cell invasion, proliferation, and death. Functions in many cellular processes including differentiation, adhesion, and signal transduction. Suppression of cancer cell motility and metastasis. Communication of cells with their microenvironment. Regulation of cell growth, differentiation and metabolism. Molecular chaperones with roles in stabilizing and folding other proteins. Association with a variety of pathogenic states. Transcriptional activators for liver-specific genes. Maintenance of glucose and lipid homeostasis. Suppressor of tumor metastasis by inhibition of EMT. Regulation of cell proliferation, cell migration and cellmatrix interactions. Activation of the complement cascade. Inhibition of cell growth and invasion. Implication of biological processes including cell adhesion, differentiation, migration, signaling, neurite outgrowth and metastasis. Regulation of cell growth and endoplasmic reticulum stress-induced cell death. Protein transport through the early secretory pathway. Regulation of immune response. Inhibition of cell cycle. Suppression of tumorigenesis. Regulation of actin polymerization. Implication of cell proliferation, migration, and differentiation Anti-inflammatory factor. Promotion of angiogenesis. Catalyzing the conversion of LPC to phosphatidylcholine (PC) in the remodeling pathway of PC biosynthesis. Promotion of cell growth. Refere.
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