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Fig. 7 | Applied Network Science

Fig. 7

From: NETME: on-the-fly knowledge network construction from biomedical literature

Fig. 7

a Depicts the pathway constructed by hand from the selected papers (Jiang et al. 2014; Kong et al. 2014; Ke et al. 2012; Grass and Toole 2016; Xiong et al. 2014; Rucci et al. 2010; Ding et al. 2017; Ulrich and Pillat 2020; Wang et al. 2014; Kong et al. 2014; Kirk et al. 2000), with CD147(BSG) as the central node. b Shows the molecular mechanisms summarised in the knowledge network developed by NETME in accordance with the same papers used in a NETME shows that CD147 is a potent inducer of metalloproteinases (MMPs) such as MMP2, MMP14 and MMP9 as reported in Xiong et al. (2014); Rucci et al. (2010); Ding et al. (2017). Furthermore, the overexpression of CD147, which results in increased phosphorylation of PI3K(PIK3CA), Akt(AKT1), leads to the secretion of vascular endothelial growth factor (VEGFA) in several biological contexts such as KSHV infection Xiong et al. (2014); Rucci et al. (2010). In addition to its ability to induce MMPs, CD147 regulates spermatogenesis, lymphocyte reactivity and MCT system, in particular MCT1 and MCT4 (MCTS1 and SLC16A4) expression (Xiong et al. 2014; Kirk et al. 2000). Our results also show that CD147 can increase the expression of ATP-binding cassette transporter G2 (ABCG2) protein, regulating its function as a drug transporter, as mentioned by Xiong et al. for MCF-7 cells (Xiong et al. 2014). NETME identifies also BSG as an upstream activator of STAT3, highlighting its involvement in tumor development in agreement with the literature (Wang et al. 2014). As summarized by our knowledge network, CD147 is regulated by various inflammatory mediators, such as RANKL (TNFSF11), denoting its involvement in inflammatory processes (Grass and Toole 2016; Rucci et al. 2010). Among the potential activators of BSG, NETME also find the transcription factor c-Myc (MYC) (Kong et al. 2014)

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