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Overexpression of miR-592 promotes GC proliferation, migration, and invasion and induces the EMT via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2, suggesting a potential therapeutic target for Gastric cancer.
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nuclear Spry2 acts as a molecular link which co-ordinates airway and vascular growth of the cardiopulmonary system.
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activation of ERK1/2 signaling was required for hCG-induced up-regulation of SPRY2 expression. Further, SPRY2 knockdown attenuated the AREG-induced COX-2 expression and PGE2 production by inhibiting AREG-activated ERK1/2 signaling.
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Result demonstrated that SPRY2 low-expression was significantly associated with unfavorable prognosis of gastric adenocarcinoma and that SPRY2 could inhibit FGFR2-induced ERK phosphorylation and suppress FGFR2-elicited gastric cancer cell proliferation and invasion.
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Sprouty2 inhibits amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.
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Sprouty2 (Spry2), a negative regulator of the extracellular signal regulated kinase/mitogen-activated protein kinase (Erk/MAPK) signalling pathway, was a downstream target of miR-122-5p possibly involved in regulating the keratinocyte proliferation.
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results shows the involvement of Spry2 in regulation of FosB and Runx2 genes, MAPK signaling and proliferation of mesenchymal stem cells.
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MYB acts on MAPK signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2.
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ZEB1 upregulation by SPRY2 results from the combined induction of ETS1 transcription factor and the repression of microRNAs (miR-200 family, miR-150) that target ZEB1 RNA. Moreover, SPRY2 increased AKT activation by epidermal growth factor, whereas AKT and also Src inhibition reduced the induction of ZEB1.
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upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells.
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In cells harbouring a K-Ras mutation the serine conversion weakens the reduction of migration velocity indicating that dependent on the status of K-Ras the serine influences Sprouty2 functions differently.
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Increased nuclear localization of p21(WAF1/CIP1) in SPRY2 downregulated colon cancer cells may explain the inhibition of cell proliferation in colon cancer cells.
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Data suggest a common mechanism by which DNA methyltransferase1 (DNMT1) and hypoxia inducible factors HIF1alpha/HIF2alpha regulate Sprouty2 (Spry2) transcription.
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We showed that Spry2 is a novel unfolded protein response target and its upregulation is dependent on PERK.
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has an inhibitory role in TGFbeta signaling pathway in lens epithelial cells
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these results establish SPRY2 as a critical negative regulator of BCR-mediated MAPK-Erk signaling in chronic lymphocytic leukemia , thereby providing one of the molecular mechanisms to explain the clinical heterogeneity of chronic lymphocytic leukemia.
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spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo.
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data suggest that Spry2 acts as a scaffold to bring more pVHL/associated E3 ligase in proximity of HIF1alpha and increase its ubiquitylation and degradation. This represents a novel action for Spry2 in modulating biological processes regulated by HIFalpha subunits.
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MiR-122 could act as a tumor promoter and potentially target Sprouty2. MiR-122 promotes renal cell carcinoma cell proliferation, migration, and invasion.
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miR27b promotes the migration and invasion of gastric cancer cells via inhibition of SPRY2mediated ERK signaling.
