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Sox2

The IVF-Generated Human Embryonic Microenvironment Reverses Progestin Resistance in Endometrial Cancer Cells by Inducing Cancer Stem Cell Differentiation

[Cancer Letters] Scientists found that progestin resistance of endometrial CSCs could be improved or reversed by using in vitro fertilization (IVF)-generated embryonic sac-derived fluid containing the embryonic microenvironment.

Prognostic Significance of NT5E/CD73 in Neuroblastoma and Its Function in CSC Stemness Maintenance

[Cell Biology and Toxicology] Researchers investigated its expression profile in neuroblastoma (NB), its association with NB clinical outcomes, and its influence in the regulation of cancer stem cells’ (CSCs) stemness maintenance.

Reg4 Interacts with CD44 to Regulate Proliferation and Stemness of Colorectal and Pancreatic Cancer Cells

[Molecular Cancer Research] Researchers identified the cell surface binding partner of Reg4 and dissected its role in colorectal cancer (CRC) and pancreatic cancer (PC) growth and stem cell survival. In vitro models of human CRC and PC were used to evaluate the results.

Long Noncoding RNA AK023096 Interacts with hnRNP-K and Contributes to the Maintenance of Self-Renewal in Bladder Cancer Stem-Like Cells

[Experimental Cell Research] Scientists investigated the expression profile and biological function of lncRNAs in urothelial cancer stem-like cells by microarray analysis.

Competitive Binding of E3 Ligases TRIM26 and WWP2 Controls SOX2 in Glioblastoma

[Nature Communications] Investigators identified E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for glioblastoma stem cells identity and maintenance.

Inability to Switch from ARID1A-BAF to ARID1B-BAF Impairs Exit from Pluripotency and Commitment towards Neural Crest Formation in ARID1B-Related Neurodevelopmental Disorders

[Nature Communications] ARID1B-BAF regulated exit from pluripotency and lineage commitment by attenuating thousands of enhancers and genes of the NANOG and SOX2 networks. In iPSCs, these enhancers were maintained active by ARID1A-containing BAF.

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