Tag results:
PI3K
Mammary Cell News
New Advances in Targeted Therapy of HER2-Negative Breast Cancer
[Frontiers in Oncology] The authors describe the potential targets that may be used for breast cancer treatment from the aspects of PI3K/AKT signaling pathway, DDR, angiogenesis, the cell cycle, breast cancer stem cells, etc
Mammary Cell News
GNG2 Acts as a Tumor Suppressor in Breast Cancer through Stimulating MRAS Signaling
[Cell Death & Disease] GNG2 over-expression could significantly block the cell cycle, inhibit proliferation, and promote apoptosis in breast cancer cells in vitro.
Mesenchymal Cell News
Ascorbic Acid 2-Glucoside Preconditioning Enhances the Ability of Bone Marrow Mesenchymal Stem Cells in Promoting Wound Healing
[Stem Cell Research & Therapy] In a wound healing mouse model, the histological evaluation of wound tissue in PBS, bone marrow MSCs (BMSCs), and ascorbic acid 2-glucoside-treated BMSCs group were investigated.
Pancreatic Cell News
Calcineurin/NFATc2 and PI3K/AKT Signaling Maintains β-Cell Identity and Function during Metabolic and Inflammatory Stress
[iScience] Scientists showed that intracellular Ca2+ and reactive oxygen species signals generated by high glucose and cytokine-induced endoplasmic reticulum stress activated calcineurin/NFATc2 and PI3K/AKT to maintain β-cell identity and function.
Endothelial Cell News
Extracellular Vesicles Enriched with an Endothelial Cell Pro-Survival microRNA Impacts Skin Tissue Regeneration
[Molecular Therapy-Nucleic Acids] Using a streptozotocin-induced diabetic wound healing mouse model, investigators showed that, compared with miR-scrambled-modulated small extracellular vesicles (sEVs), topical administration of miR-425-5p-modulated sEVs significantly enhanced wound healing, a process mediated by enhanced vascularization and skin re-epithelialization.
Prostate Cell News
GNE-493 Inhibits Prostate Cancer Cell Growth via Akt-mTOR-Dependent and -Independent Mechanisms
[Cell Death Discovery] A constitutively-active mutant Akt1 restored Akt-mTOR activation but only partially ameliorated GNE-493-induced prostate cancer cell death. Moreover, GNE-493 was still cytotoxic in Akt1/2-silenced primary prostate cancer cells.