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STAT3

Golgi Phosphoprotein 3 Promotes Colon Cancer Cell Metastasis Through STAT3 and Integrin α3 Pathways

[Frontiers in Molecular Biosciences] In vitro genetic ablation of golgi phosphoprotein 3 (GOLPH3) was performed using small interfering RNA transfection, and a stably overexpressed GOLPH3 colon cancer cell line was constructed using the lentivirus system.

Zinc Complex of 3,5-Di-Tert-Butyl Salicylate Inhibits Viability, Migration, and Invasion in Triple-Negative Breast Cancer Cells

[Scientific Reports] Investigators found that the zinc complex of 3,5-di-tert-butyl salicylate compound inhibited viability, invasion, and migration and induced apoptosis in triple-negative breast cancer 4T1 cells.

IL-6/JAK/STAT3 Signaling in Breast Cancer Metastasis: Biology and Treatment

[Frontiers in Oncology] The authors cover the current biological understanding of the interleukin-6 (IL-6) signaling pathway and its impact on breast cancer metastasis, as well as, therapeutic interventions that target components of the IL-6 pathway.

Deletion of STAT3 from Foxd1 Cell Population Protects Mice from Kidney Fibrosis by Inhibiting Pericytes Trans-differentiation and Migration

[Cell Reports] Signal transduction and activator of transcription 3 (STAT3) activation increased migration and profibrotic signaling in genome-edited, pericyte-like cells. Conversely, blocking Stat3 inhibited detachment, migration, and profibrotic signaling.

Lon Upregulation Contributes to Cisplatin Resistance by Triggering NCLX-Mediated Mitochondrial Ca2+ Release in Cancer Cells

[Cell Death & Disease] Scientists reported the role of Lon in the response to cisplatin-induced mtDNA damage and oxidative stress, which conferred cancer cells on cisplatin resistance via modulating calcium levels in mitochondria and cytosol.

Inhibition of Proinflammatory Signaling Impairs Fibrosis of Bone Marrow Mesenchymal Stromal Cells in Myeloproliferative Neoplasms

[Experimental & Molecular Medicine] Scientists showed that bone marrow-derived MSCs contributed to fibrosis in myeloproliferative neoplasms by differentiating into αSMA-positive myofibroblasts.

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