Later, it was found that direct focuses on of miR-491-5p are and and (PI3K/AKT/mTOR pathway), miR-7 induces apoptosis and suppresses tumor growth in in vivo experiments [36]. chemoresistance, in most cases, impact the regulators of apoptosis and are associated with the PI3K/AKT/mTOR pathway. The characteristics of microRNAs proposed as candidates for GC biomarkers were analyzed. The currently developed diagnostic and prognostic panels of microRNAs will also be regarded as. and that inhibit the metalloproteinases. This activates PI3K/AKT/mTOR and a number of signaling pathways with which metalloproteinases interact. Some microRNAs can simultaneously become activators of one pathway and blockers of another. Thus, miR-216a blocks the JAK/STAT and Wnt/-catenin pathways, inhibiting and the TGF- pathway mediator. Moreover, by inhibiting one target, microRNAs can take action on two signaling pathways. These microRNAs include miR-592, which, by suppressing its target and and prospects to activation of metalloproteinases and damage of the extracellular matrix and basement membrane of cells, which are predictors of the metastatic process [21,22,23,24,25,26,27]. These microRNAs, by inhibiting numerous focuses on, impact a number of signaling pathways, which leads to the suppression of apoptosis and promotes the development of metastases. MiR-302b is definitely a suppressor of tumor growth and metastasis in Flucytosine GC. A decreased level of miR-302b manifestation is associated with the involvement of regional lymph nodes in the metastatic process, peritoneal carcinomatosis, and the development of distant metastases. Direct targets of miR-302b include and leads to the activation of EGFR and signaling pathways PI3K/AKT/mTOR and RAS/RAF/ERK/MAPK. This activates the ATP-binding cassette transporter P-gp (ABCB1), which causes an increase in the outflow of medicines from your cell. In addition, the anti-apoptotic protein BCL2 is also induced. The gene is definitely another target of miR-20a. Suppression of activates the NF-B signaling pathway and anti-apoptotic proteins Livin and Survivin. Due to the action of these mechanisms, miR-20a overexpression caused an increase in the efflux of chemotherapy medicines from cultured Flucytosine GC cells, as well as apoptosis suppression, which led to the development of tumor cell chemoresistance [31,32]. Decreased miR-20a manifestation was shown to inhibit Wnt/-catenin and RAS/RAF/ERK/MAPK signaling pathways. This, in turn, led to inhibition of growth, as well as the invasive and migratory properties of GC Flucytosine cells by in vitro experiments [33]. In experiments on GC cell lines, miR-491-5p suppressed cell migration and proliferation and advertised apoptosis. MiR-491-5p was originally described as an inhibitor of the antiapoptotic element BCL-XL. MiR-491-5p offers been shown to inhibit ERK1/2 and AKT. Later, it was found that direct focuses on of miR-491-5p are and and (PI3K/AKT/mTOR pathway), miR-7 induces apoptosis and suppresses tumor growth in in vivo experiments [36]. As a result of suppression of its target RELA, miR-7 inhibits the NF-B signaling pathway and genes associated with metastasis: [37]. In Zhao et al., miR-7 was identified as a direct inhibitor of and genes, in addition to the rules of cell proliferation, are involved in the mechanisms of cell migration. IGF1R is definitely a predictor of neoplastic transformation and is involved in key stages of the metastatic cascade, such as adhesion, migration, invasion, colonization by tumor Flucytosine cells of distant organs, and angiogenesis. In experiments on GC cell lines, SNAIL was inhibited as a result of suppression of IGF1R, which led to the activation of E-cadherin and suppression of EMT [38]. Thus, by obstructing the IGF/IGF1R/IRS1 signaling pathway, and others mentioned above, miR-7 is an inhibitor of EMT and metastatic processes in GC. The genes have been identified as direct focuses on of miR-1271 in GC [39]. and PKX1 belong to the IGF/IGF1R/IRS1 signaling pathway, which is definitely often considered as part of the PI3K/AKT/mTOR pathway and is Flucytosine involved in the rules of cell proliferation and apoptosis [40]. IGF/IGF1R/IRS1 is an activator of the PI3K/AKT/mTOR pathway. As a result of PI3K/AKT/mTOR activation, the antiapoptotic protein BCL2 is definitely induced [41]. Therefore, by acting on a number of.