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PTEN

Brain Endothelial PTEN/AKT/NEDD4-2/MFSD2A Axis Regulates Blood-Brain Barrier Permeability

[Cell Reports] Scientists showed that cerebrovascular endothelial cell-specific deletion of Pten resulted in a dramatic increase in vesicular transcytosis by the reduction of major facilitator superfamily domain-containing 2a, leading to increased transcellular permeability of the blood-brain barrier.

Long Non-Coding RNA BRE-AS1 Inhibits the Proliferation, Migration, and Invasion of Cancer Cells in Triple-Negative Breast Cancer and Predicts Patients’ Survival by Downregulating miR-21

[BMC Cancer] BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of long non-coding RNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes.

Kras Activation in Endometrial Organoids Drives Cellular Transformation and Epithelial-Mesenchymal Transition

[Oncogenesis] Investigators found that in KrasG12D-expressing endometrial organoids, Pten knockdown did not confer tumorigenicity, but Cdkn2a knockdown or Trp53 deletion led to the development of carcinosarcoma, a rare, aggressive tumor comprising both carcinoma and sarcoma.

Reactivation of the Tumor Suppressor PTEN by mRNA Nanoparticles Enhances Antitumor Immunity in Preclinical Models

[Science Translational Medicine] Investigators demonstrated that mRNA delivery by polymeric nanoparticles could effectively induce expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in Pten-mutated melanoma cells and Pten-null prostate cancer cells, which in turn induced autophagy and triggered cell death–associated immune activation via release of damage-associated molecular patterns.

Targeting Therapy-Resistant Lung Cancer Stem Cells via Disruption of the AKT/TSPYL5/PTEN Positive-Feedback Loop

[Communications Biology] Researchers identified testis-specific Y-like protein 5 (TSPYL5) as an upstream regulator of CSC-associated genes in non-small cell lung cancer cells, and suggested this as a therapeutic target for CSC elimination.

BRN2 Is a Non-canonical Melanoma Tumor-Suppressor

[Nature Communications] In a BrafV600E PtenF/+ context, researchers showed that BRN2 haplo-insufficiency promoted melanoma initiation and metastasis.

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