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AKT

PIK3R3, Part of the Regulatory Domain of PI3K, Is Upregulated in Sarcoma Stem-Like Cells and Promotes Invasion, Migration, and Chemotherapy Resistance

[Cell Death & Disease] To identify drivers of sarcoma cancer stem-like cells, the authors compared gene expression using RNA sequencing between HT1080 fibrosarcoma and SK-LMS-1 leiomyosarcoma spheroids compared with the parent populations.

A Novel Chemical Inhibitor Suppresses Breast Cancer Cell Growth and Metastasis through Inhibiting HPIP Oncoprotein

[Cell Death Discovery] The authors screened compounds inhibiting breast cancer cell proliferation with hematopoietic PBX-interacting protein (HPIP) fused with green fluorescent protein as a reporter. A novel agent named TXX-1-10 derived from rimonabant was discovered to reduce HPIP expression and had greater inhibitory effects on breast cancer cell growth and metastasis in vitro and in vivo than rimonabant.

Single-Cell Immunoblotting Resolves Estrogen Receptor-α Isoforms in Breast Cancer

[PLoS One] To scrutinize hormone response heterogeneity among breast cancer (BCa) tumor cells, scientists developed a precision tool to specifically measure estrogen receptor alpha (ER-α)-66, ER-α46, and eight ER-signaling proteins with single-cell resolution in the highly hetero-clonal MCF-7 BCa cell line.

Tonkinensine B Induces Apoptosis through Mitochondrial Dysfunction and Inactivation of the PI3K/AKT Pathway in Triple-Negative Breast Cancer Cells

[Journal of Pharmacy and Pharmacology] With the help of cell cytotoxicity, the effect of tonkinensine B on MDA-MB-231 cells was investigated. The levels of key apoptosis-associated proteins Bcl-2, Bax, caspase-9, caspase-3 and AKT in MDA-MB-231 cells were analysed to determine whether tonkinensine B caused apoptosis via the mitochondrial pathway.

B-Myb Accelerates Colorectal Cancer Progression through Reciprocal Feed-Forward Transactivation of E2F2

[Oncogene] B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo.

ERBB3 Overexpression Due to miR-205 Inactivation Confers Sensitivity to FGF, Metabolic Activation, and Liability to ERBB3 Targeting in Glioblastoma

[Cell Reports] Researchers identified a human glioblastoma subset characterized by ERBB3 overexpression and nuclear accumulation.

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