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EMT

Cancer Stem Cell Marker DCLK1 Reprograms Small Extracellular Vesicles toward Migratory Phenotype in Gastric Cancer Cells

[Proteomics] The authors reported that doublecortin‐like kinase 1 (DCLK1) influences small extracellular vesicle biogenesis in a kinase‐dependent manner.

Inverse Agonism at the Na/K‐ATPase Receptor Reverses EMT in Prostate Cancer Cells

[Prostate] The authors showed that the loss of cell surface expression of Na/K‐ATPase α1 induced epithelial–mesenchymal transition and promoted metastatic potential and tumor growth of prostate cancer by decreasing the expression of E‐cadherin and increasing c‐Myc expression via the activation of Src/FAK pathways.

PLK1/Vimentin Signaling Facilitates Immune Escape by Recruiting Smad2/3 to PD-L1 Promoter in Metastatic Lung Adenocarcinoma

[Cell Death & Differentiation] Researchers showed that vimentin phosphorylated by PLK1, triggered TGF-β-signaling, which consequently led to metastasis and PD-L1 expression for immune suppression in lung adenocarcinoma.

Adipocyte-Like Signature in Ovarian Cancer Minimal Residual Disease Identifies Metabolic Vulnerabilities of Tumor Initiating Cells

[JCI Insight] Investigators performed dense multi-region transcriptomics analysis of paired biopsies from 17 ovarian cancer patients before and after chemotherapy.

MDM2 Induces EMT via the B-Raf Signaling Pathway through 14-3-3

[Oncology Reports] Scientists demonstrated that the expression levels of MDM2 proto‑oncogene, E3 ubiquitin protein ligase were markedly increased in TGF‑β‑induced epithelial‑to‑mesenchymal transition using quantitative PCR and western blotting.

The Oncogenic E3 Ligase TRIP12 Suppresses Epithelial–Mesenchymal Transition (EMT) and Mesenchymal Traits through ZEB1/2

[Cell Death Discovery] Investigators explored thyroid hormone receptor interactor 12's role in the inhibition of epithelial-mesenchymal transition and implied a potential suppressive role in breast cancer metastasis.

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