Investigators showed that breast cancer cells maintained in hypoxia releasee small extracellular vesicles that activated mitochondrial dynamics, stimulated mitochondrial movements, and promoted organelle accumulation at the cortical cytoskeleton in normal mammary epithelial cells.
Based on the methods for isolating and identifying cancer stem cells and the functional features of long-term tumor-initiating cells (LT-TICs), the authors aimed to identify a subpopulation of LT-TICs.
Loss of function studies of PIAS1 and TIF1γ suggested that these E3 ligases act in an interdependent manner to suppress epithelial–mesenchymal transition of breast cell-derived tissue organoids. The authors unveiled a novel mechanism by which SUMO E3 ligases coordinate substrate SUMOylation with biological implications.
[Cell Death & Differentiation]
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Scientists showed that AU-rich element RNA-binding protein 1 was an important inducer of the epithelial-to-mesenchymal transition process through stabilization of SNAIL1 and TWIST1 and the consequent promotion of breast cancer stem cells.
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AUF1 promotes stemness in human mammary epithelial cells through stabilization of the EMT transcription factors TWIST1 and SNAIL1 | Oncogenesis. (n.d.). Retrieved August 6, 2020, from https://www.nature.com/articles/s41389-020-00255-1 Cite
To identify hepatocellular carcinoma (HCC) signaling networks that determine responses to kinase inhibitors (KIs), scientists applied a pharmacoproteomics approach integrating kinome activity in 17 HCC cell lines with their responses to 299 KIs, resulting in a comprehensive dataset of pathway-based drug response signatures.
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Researchers showed that AUF1 induced epithelial-to-mesenchymal transition and stemness in breast epithelial cells via stabilization of the SNAIL1 and TWIST1 mRNAs, and their consequent upregulation.
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Investigators found that overexpression of Go-Ichi-Ni-San 2 (GINS2) contributed to advanced clinical stage of pancreatic cancer patient and promoted epithelial–mesenchymal-transition in vitro and in vivo via specifically activating ERK/MAPK signal pathway.
[Cancer Gene Therapy]
In vitro and in vivo functional studies performed by silencing or overexpressing TET1 suggested that TET1 was able to suppress epithelial-mesenchymal transition and sensitize pancreatic ductal adenocarcinoma cells to 5FU and gemcitabine. RNA-seq, whole genome bisulfite sequencing and ChIP-seq were used to explore the TET1-associated pathway, and showed that TET1 promoted the transcription of CHL1 by binding and demethylating the CHL1 promoter, which consequently inhibits the Hedgehog pathway.
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Li, H., Jiang, W., Liu, X.-N., Yuan, L.-Y., Li, T.-J., Li, S., Xu, S.-S., Zhang, W.-H., Gao, H.-L., Han, X., Wang, W.-Q., Wu, C.-T., Yu, X.-J., Xu, H.-X., & Liu, L. (2020). TET1 downregulates epithelial-mesenchymal transition and chemoresistance in PDAC by demethylating CHL1 to inhibit the Hedgehog signaling pathway. Oncogene, 1–14. https://doi.org/10.1038/s41388-020-01407-8 Cite
Investigators evaluated the growth of moderate differentiated colorectal cancer from LGR5-positive cells, which was a cancer stem cell marker of colorectal cancer, using xenograft and three-dimensional culture models spatiotemporally.
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LINC00941 was found to activate EMT by directly binding the SMAD4 protein MH2 domain and competing with β-TrCP to prevent SMAD4 protein degradation, thus activating the TGF-β/SMAD2/3 signaling pathway.
[Cell Death & Differentiation]
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This study investigated the effects of H4R ligands on epithelial-mesenchymal transition and mammosphere formation as a surrogate assay for cancer stem cells in breast cancer cells with different invasive phenotype. They also investigated the participation of Src and TGF-β signaling in these events.
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The authors reconstituted PTEN-deficient breast cancer cells with wild-type and mutant PTEN, demonstrating that restoration of PTEN expression converted cancer cells with mesenchymal traits to an epithelial phenotype and inhibited cancer stem cell activity.
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