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"Curcumin inhibited BCSCs migration by inhibiting beta-catenin nuclear translocation, attenuating the expression of beta-catenin transcriptional targets including pro EMT factors, along with the increased formation of E, cadherin, beta, and catenin complex and suppressed expression of epithelial markers."
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"Wang et al. reported that an increase in mRNA expression of beta-catenin and axin2 in kidney tissues of patients with lupus nephritis compared with control kidney tissues, accompanied by an increase of beta-catenin protein expression XREF_BIBR Their study also showed that beta-catenin mRNA expression was significantly higher in lupus nephritis patients without renal interstitial fibrosis compared to those with renal interstitial fibrosis and increased beta-catenin mRNA expression positively correlated with the creatinine clearance rate (Ccr)."
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"We also showed that CENPK was directly bound to SOX6 and disrupted the interactions of CENPK with β-catenin, which promoted β-catenin expression and nuclear translocation, facilitated p53 ubiquitination, and led to activation of Wnt/β-catenin signaling, but suppression of the p53 pathway."
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"More important, knockdown of beta-catenin through siRNA not only markedly inhibited the expression of beta-catenin as well as its downstream targets c-Myc and cyclinD1 (XREF_FIG H-I), but also abrogated the effects of CBX4 on cell growth and colony formation in soft agar (XREF_FIG J-L)."
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"These results were supported by Western analysis, in which beta-catenin knockdown in mice subjected to Ad-HO-1 or Ad-IL-10 diminished the expression of beta-catenin (XREF_FIG, 0.2-0.5 AU) in the ischemic liver lobes, whereas NS siRNA followed by Ad-HO-1 or Ad-IL-10 did not affect beta-catenin levels (2.0-2.3 AU)."
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"The increased concentration of beta-catenin protein in the cytoplasm favors its translocation to the nucleus as a coactivator for the TCF/LEF (T-cell factor and lymphoid enhancer factor) family and activates the transcription of Wnt and beta-catenin target genes, such as c-myc and cyclin D1, which function as oncogenes XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."
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"Suppression of the transactivation effects of beta-catenin and Tcf with FH535 ((N-(2-methyl-4-nitro) -2,4-dichlorosulfonamide, a beta-catenin and Tcf inhibitor) significantly decreased the protein levels of beta-catenin and METTL3, and then increased the levels of pp53, in TP53-Dox cells (XREF_FIG)."
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"The present observation that the inhibitor of beta-catenin signaling, XAV939, impairs not only the amount of active beta-catenin but also the expression of PFKP in a manner similar to that of WNT5A signaling supports the idea that WNT5A impairs aerobic glycolysis in breast cancer cells via reduced beta-catenin signaling."
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"Portal-Nunez et al. [XREF_BIBR] also observed the STZ induced DM rat models with the parathyroid treatment group as the control, using the gene chip technology and rt-PCR analysis of Wnt and beta-catenin signal pathway change and analysis of beta-catenin protein expression by immunohistochemical method change."
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"According to the results (Fig. 4a), 0.25, 0.5, 0.75, and 1 μg siRNA interfered with β-catenin expression, of which 0.5 μg siRNA significantly lowered β-catenin expression (p < 0.05) compared to 0.25 μg siRNA, while 0.5, 0.75, and 1 μg siRNA did not significantly downregulate β-catenin expression."
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"Interestingly, Akt1 gene silencing in HLEC resulted in the increased presence of β-catenin in the cytosol and nucleus from its normal localisation in the endothelial adherens junctions, and treatment with ICG001 and IWR-1 that prevent β-catenin nuclear localisation restored β-catenin expression in the cell–cell junctions (Fig. 2e; Supplemental Fig. 1A)."
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"In AML, MUC1-C associates with the beta, catenin, and TCF4 complex, which regulates cell proliferation and differentiation.5, 12 Accumulation of beta-catenin in the cytoplasm promotes its translocation to the nucleus as a cofactor for transcription factors of the T-cell factor (TCF) family and activates the transcription of Wnt and beta-catenin target genes."
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"By comparison in colonic adenocarcinomas, elevated beta-catenin levels caused by mutations in CTNNB1 or APC result in activation of the Wnt/beta-catenin/LEF1 pathway through a LEF1 binding site in the cyclin D1 promotor, triggering cyclin D1 gene expression, and subsequently, uncontrolled progression of tumor cells into the cell cycle [XREF_BIBR, XREF_BIBR]."
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"As beta-catenin functions as a transcriptional co-activator to promote cell proliferation after being transported into the nucleus [XREF_BIBR, XREF_BIBR], we guess that the increased beta-catenin and active-beta-catenin in the nucleus after YAP over-expression may promote the transcription of beta-catenin target genes."
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"Moreover, the cytoplasmic and nuclear accumulation of beta-catenin could be observed in premalignant lesions (atrophic gastritis and IM) [XREF_BIBR], and increased beta-catenin mRNA levels and mutational alterations of the APC and beta-catenin gene are present in intestinal-type GC [XREF_BIBR]."
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"Furthermore, β-catenin IHC staining demonstrated that subcutaneous tumors formed by full-length SPINT1-AS1 overexpressed HeLa cells had increased β-catenin expression compared with those formed by control HeLa cells, which was largely reversed by the deletion of DNM3OS binding site on SPINT1-AS1 (Figure 6E)."
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"Nuclear expression of beta-catenin was down-regulated in LN229 and U87 glioma cells by a small molecule inhibitor of beta-catenin and TCF4 signaling, demonstrating strongly inhibited beta-catenin and TCF4 transcriptional activity and STAT3 luciferase activity, as well as decreased mRNA and protein levels of nuclear beta-catenin, TCF4, EGFR, AKT1, AKT2 and STAT3."
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"Three small molecules -- Inhibitor of beta-Catenin And TCF4 (ICAT), niclosamide, and XAV939 -- have been shown to strongly and specifically reduce levels of active beta-catenin in vitro by inhibiting beta-catenin stabilization and downstream beta-catenin signaling (TCF/LEF reporter activity)."
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"Accordingly, we previously demonstrated that over-expression of beta-catenin slightly activates Tcf/Lef mediated transcription in melanocyte lineages XREF_BIBR but is not sufficient to prime the melanogenic program XREF_BIBR, suggesting that even if beta-catenin could synergize with other pathways the exclusive presence of a large amount of nuclear beta-catenin is not sufficient to activate the melanogenic program."
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"Stabilization of beta-catenin in proximal epithelium using the Catnb floxedExon3 allele raised epithelial beta-catenin levels, resulting in squamous, cuboidal, and goblet cell dysplasia in intrapulmonary conducting airways and the appearance of alveolar type 2 like cells in the bronchioles."
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"It is believed that accumulation of beta-catenin in the cytoplasm favors its translocation to the nucleus as a cofactor for transcription factors of the T-cell factor and lymphoid enhancing factor (TCF/LEF) family and activates the transcription of Wnt and beta-catenin target genes, which regulates cell proliferation and differentiation [XREF_BIBR]."
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"We found that PAK7 overexpression dramatically up-regulated the expression of beta-catenin, p-GSK3beta (S9) and downstream target genes cyclin D1 and c-myc, but did n't affect protein expression level of GSK-3beta in MCF-7 cells, besides that, the expression of beta-catenin and c-myc in nucleus also increased."
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"Furthermore, Yang et al. reported that Wnt3a, a representative canonical member of the Wnt family of ligands, upregulates the expression of beta-catenin and enhances the osteogenic differentiation of dental follicle cells, while dickkopf1, a Wnt and beta-catenin signalling inhibitor, decreases the expression of beta-catenin and attenuates the osteogenic differentiation of dental follicle cells 13."
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"Furthermore, CGP049090, a small molecule inhibitor of Wnt and beta-catenin, inhibited the expression of beta-catenin (5 microM, P = 0.0227; 10 microM, P = 0.0086), c-myc (5 microM, P = 0.0213; 10 microM, P = 0.0017) and cyclin D1 (5 microM, P = 0.0243; 10 microM, P = 0.0033) in MG63 cells in a concentration dependent manner (XREF_FIG)."
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"Notably, abnormal activation of the Wnt and beta-catenin signaling pathway leads to beta-catenin accumulation in the nucleus and subsequent binding to the T cell factor (TCF) or lymphoid enhancer factor (LEF) transcription factors, thereby inducing the expression of Wnt and beta-catenin target genes, which are essential for EMT and metastatic progression of epithelial cancers."
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"Real-time PCR and Western blot assay at 48 h after infection showed that CTNNB1 knockdown in A-498 cells significantly decreased the mRNA and protein levels of CTNNB1 (XREF_FIG), whereas overexpression of CTNNB1 in 786-O (XREF_FIG) and ACHN cells (XREF_SUPPLEMENTARY) significantly increased the mRNA and protein levels of CTNNB1."
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"Addition of both Wnt5a and calcium to NHEKs activated the Wnt and beta-catenin signaling pathway as indicated by (i) increased stability of beta-catenin in the cells, (ii) enhanced beta-catenin transcriptional activity, demonstrated by a luciferase based beta-catenin-activated reporter assay, and (iii) augmented Wnt and beta-catenin target gene expression."
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"It is believed that accumulation of beta-catenin in the cytoplasm favours its translocation to the nucleus as a cofactor for transcription factors of the T-cell factor and lymphoid enhancing factor (TCF/LEF) family and activates the transcription of Wnt and beta-catenin target genes, which are involved in cellular differentiation and proliferation (Giles et al, 2003)."
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"Moreover, knockdown of OPN significantly decreased the protein levels of p-MEK, p-MAPK1, and beta-Catenin, OPN up-regulation distinctly activated the MEK and MAPK pathway and beta-Catenin expression in RBE cells, and this activation of MEK and MAPK pathway was abrogated by MEK inhibitor U0126."
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"Our model shows that (1) Pdcd4 knock-down leads to down-regulation of E-cadherin through up-regulating Snail expression, (2) decreased E-cadherin expression changes cell morphology and releases beta-catenin, and (3) the free beta-catenin then translocates into the nucleus, binds to Tcf4 transcription factors, and activates beta-catenin and Tcf dependent transcription to stimulate the expression of u-PAR and c-Myc, which promote tumor cell invasion (XREF_FIG)."
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"And most importantly, Wnt and beta-catenin signaling pathway activation by overexpression of beta-catenin not only significantly reversed the anti-proliferation and induction apoptosis of baicalein, but also attenuated the baicalein induced motility restriction, indeed promoting its motile ability."
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"In Wnt dependent cancers, Wnt pathways are aberrantly activated by mutational mechanisms, including the inactivation of APC or AXIN, or by activating mutations in beta-catenin, all of which lead to constitutive transcription of beta-catenin and TCF-regulated genes [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Since beta-catenin (CTNNB1) is an important regulator of the Wnt and beta-catenin signaling pathway, and many transcriptional regulators have been shown to regulate the transcription of CTNNB1, nuclear MYH9 induced CTNNB1 transcription in GC cells found in this study further contributed to our understanding of the mechanisms regulating the transcription of CTNNB1."
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"The aims of this study were to address the distribution of beta-catenin expression in invasive breast cancers, the correlations between beta-catenin expression and clinicopathological features and survival of breast cancer patients, and to determine whether aberrant beta-catenin expression is driven by CTNNB1 (beta-catenin encoding gene) activating mutations."