We are analyzing https://link.springer.com/article/10.1186/1471-2407-11-49.

Title:
Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters | BMC Cancer
Description:
Background Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. Methods In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. Results We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Conclusions Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.
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Keywords {🔍}

cells, βcatenin, expression, cancer, stem, emt, article, cell, hela, pubmed, akt, twist, activation, mcf, google, scholar, figure, cas, twistoverexpressing, pathway, pathways, celllike, tumor, results, luciferase, wnta, breast, properties, gskβ, found, signaling, transfectants, stable, activity, nuclear, experiments, induced, western, snail, authors, blotting, showed, medium, measured, critical, transition, formation, significantly, cscs, human,

Topics {✒️}

pre-publication history beta-catenin/lef-1 signaling pathway wnt/β-catenin pathway mediates human colon-cancer-initiating cells wnt/β-catenin signaling pathway gsk-3β phosphorylates β-catenin suggests β-catenin/tcf-4 signaling epithelial stem-cell compartments colorectal adenoma-carcinoma process improve long-term survival peroxidase-conjugated secondary antibodies β-catenin pathway plays transforming growth factor-beta epithelial-mesenchymal transition wnt/beta-catenin signaling article download pdf neural stem/progenitor cells gsk-3β mediated phosphorylaton antagonizing p53-mediated apoptosis β-catenin signaling pathway obtain wnt3a-conditioned media cell-cell adhesion molecule modulates cell-cell adhesion twist-overexpressing cell lines mesenchymal transition status twist induces stem-cell wnt/β-catenin pathway twist-overexpressing cells stimulated dual-luciferase reporter assay top/fop luciferase activities full size image dual-luciferase assay kit epithelial-mesenchymal transitions gsk-3beta-mediated phosphorylation twist-overexpressing stable transfectants mesenchymal markers n-cadherin twist activates β-catenin fundamental clinical implications released cytoplasmic β-catenin pi3k/akt inhibitors wortmannin metastatic progenitor cells nuclear β-catenin contributed gsk-3β-mediated phosphorylation t1 colorectal carcinoma related subjects top/fop luciferase activity free cytoplasmic β-catenin human pancreatic cancer twist-overexpressing cells resulted stable murine l-cells

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         description:Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.
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      headline:Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters
      description:Epithelial-mesenchymal transition (EMT) not only confers tumor cells with a distinct advantage for metastatic dissemination, but also it provides those cells with cancer stem cell-like characters for proliferation and drug resistance. However, the molecular mechanism for maintenance of these stem cell-like traits remains unclear. In this study, we induced EMT in breast cancer MCF7 and cervical cancer Hela cells with expression of Twist, a key transcriptional factor of EMT. The morphological changes associated with EMT were analyzed by immunofluorescent staining and Western blotting. The stem cell-like traits associated with EMT were determined by tumorsphere-formation and expression of ALDH1 and CD44 in these cells. The activation of β-catenin and Akt pathways was examined by Western blotting and luciferase assays. We found that expression of Twist induced a morphological change associated with EMT. We also found that the cancer stem cell-like traits, such as tumorsphere formation, expression of ALDH1 and CD44, were significantly elevated in Twist-overexpressing cells. Interestingly, we showed that β-catenin and Akt pathways were activated in these Twist-overexpressing cells. Activation of β-catenin correlated with the expression of CD44. Knockdown of β-catenin expression and inhibition of the Akt pathway greatly suppressed the expression of CD44. Our results indicate that activation of β-catenin and Akt pathways are required for the sustention of EMT-associated stem cell-like traits.
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         Cancer Stem Cell
         Wortmannin
         Salinomycin
         Tumorsphere Formation
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         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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