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EMT

An Organoid Model of Colorectal Circulating Tumor Cells with Stem Cell Features, Hybrid EMT State and Distinctive Therapy Response Profile

[Journal of Experimental & Clinical Cancer Research] Investigators generated organoids from circulating tumor cells isolated from an orthotopic colorectal cancer xenograft model.

Loss of Function of BRCA1 Promotes EMT in Mammary Tumors through Activation of TGFβR2 Signaling Pathway

[Cell Death & Disease] Researchers analyzed murine and human tumors and identified a role for Tgfβr2 in governing the molecular aspects of epithelial to mesenchymal transition that occured with Brca1 loss.

siRNA-Induced CD44 Knockdown Suppresses the Proliferation and Invasion of Colorectal Cancer Stem Cells through Inhibiting Epithelial–Mesenchymal Transition

[Journal of Cellular and Molecular Medicine] To examine the contribution of siRNA-induced knockdown of CD44 to the biological features of colorectal CSCs, colorectal CSCs HCT116-CSCs were generated, and CD44 was knocked down in HCT116-CSCs using siRNA.

Transforming Growth Factor-Beta (TGF-β) in Prostate Cancer: A Dual Function Mediator?

[International Journal of Biological Macromolecules] The authors discuss the role of TGF-β signaling in proliferation, metastasis and therapy response of prostate cancer cells and in order to improve knowledge towards its regulation, upstream mediators of TGF-β such as non-coding RNAs are described.

Numb-PRRL Promotes TGF-β1- and EGF-Induced Epithelial-to-Mesenchymal Transition in Pancreatic Cancer

[Cell Death & Disease] The authors studied the specific function of Numb-PRRL isoform in activated EMT of pancreatic ductal adenocarcinoma, which was distinguished from our previous studies that only focused on the total Numb protein.

Stathmin 1 Is a Biomarker for Diagnosis of Microvascular Invasion to Predict Prognosis of Early Hepatocellular Carcinoma

[Cell Death & Disease] Through bioinformatics analysis and clinical sample verification, investigators discovered that Stathmin 1 gene was significantly up-regulated at the locations of microvascular invasion.

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