FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells - Wikidata - wikimedia - TriplyDB

FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells

FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells

http://www.wikidata.org/entity/Q35741551

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Novel therapeutic strategies for patients with triple-negative breast cancer Overexpression of the miR-141/200c cluster promotes the migratory and invasive ability of triple-negative breast cancer cells through the activation of the FAK and PI3K/AKT signaling pathways by secreting VEGF-A The insulin-like growth factor-I receptor (IGF-IR) in breast cancer: biology and treatment strategies.Involvement of FAK-ERK2 signaling pathway in CKAP2-induced proliferation and motility in cervical carcinoma cell lines.Mesenchymal Stromal Cells Epithelial Transition Induced by Renal Tubular Cells-Derived Extracellular Vesicles Antiproliferative and apoptotic effects of a specific anti-insulin-like growth factor I receptor single chain antibody on breast cancer cells.Prolactin Promotes Breast Cancer Cell Migration through Actin Cytoskeleton Remodeling.γKlotho is a novel marker and cell survival factor in a subset of triple negative breast cancers HER2 reduces breast cancer radiosensitivity by activating focal adhesion kinase in vitro and in vivo.PCP4/PEP19 promotes migration, invasion and adhesion in human breast cancer MCF-7 and T47D cells.IGF-IR signaling in epithelial to mesenchymal transition and targeting IGF-IR therapy: overview and new insights The metastasis suppressor CD82/KAI1 inhibits fibronectin adhesion-induced epithelial-to-mesenchymal transition in prostate cancer cells by repressing the associated integrin signaling.New Treatment Opportunities in Phosphatase and Tensin Homolog (PTEN)-Deficient Tumors: Focus on PTEN/Focal Adhesion Kinase Pathway.IGF1R depletion facilitates MET-amplification as mechanism of acquired resistance to erlotinib in HCC827 NSCLC cells.When the endothelium scores an own goal: endothelial cells actively augment metastatic extravasation through endothelial-mesenchymal transition.The roles of microRNAs related with progression and metastasis in human cancers.Antitumor effect of focal adhesion kinase inhibitor PF562271 against human osteosarcoma in vitro and in vivo Glycans as Regulatory Elements of the Insulin/IGF System: Impact in Cancer Progression.The activation of SRC family kinases and focal adhesion kinase with the loss of the amplified, mutated EGFR gene contributes to the resistance to afatinib, erlotinib and osimertinib in human lung cancer cells.Function of insulin-like growth factor 1 receptor in cancer resistance to chemotherapy.Acquisition of EGFR TKI resistance and EMT phenotype is linked with activation of IGF1R/NF-κB pathway in EGFR-mutant NSCLC.Growth differentiation factor 15 mediates epithelial mesenchymal transition and invasion of breast cancers through IGF-1R-FoxM1 signaling.Whole exome sequencing identified sixty-five coding mutations in four neuroblastoma tumors.Galectin-8 induces partial epithelial-mesenchymal transition with invasive tumorigenic capabilities involving a FAK/EGFR/proteasome pathway in MDCK cells.Identification and bioinformatics analysis of miRNAs associated with human muscle invasive bladder cancer.MiR-99a suppresses proliferation, migration and invasion of esophageal squamous cell carcinoma cells through inhibiting the IGF1R signaling pathway.Let-7c inhibits migration and epithelial-mesenchymal transition in head and neck squamous cell carcinoma by targeting IGF1R and HMGA2.Mifepristone inhibits proliferation, migration and invasion of HUUA cells and promotes its apoptosis by regulation of FAK and PI3K/AKT signaling pathway Molecular Signatures of the Insulin-like Growth Factor 1-mediated Epithelial-Mesenchymal Transition in Breast, Lung and Gastric Cancers

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FAK activation is required for IGF1R-mediated regulation of EMT, migration, and invasion in mesenchymal triple negative breast cancer cells

http://www.wikidata.org/entity/Q35741551

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2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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FAK activation is required for ...... e negative breast cancer cells

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ONCOTARGET.3023

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FAK activation is required for ...... e negative breast cancer cells

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Adam Marcus

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Elaine Oberlick

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Erik Kline

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LaTonia Taliaferro-Smith

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Lauren Havel

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Ruth O'Regan

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Siobhan Donnelly

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P2860

Focal adhesion kinase (FAK) activates and stabilizes IGF-1 receptor

Twist, a master regulator of morphogenesis, plays an essential role in tumor metastasis

DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells

Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice

Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies

Required role of focal adhesion kinase (FAK) for integrin-stimulated cell migration.

Focal adhesion kinase: a regulator of focal adhesion dynamics and cell movement.

Reciprocal regulation of ZEB1 and AR in triple negative breast cancer cells.

CCN6 (WISP3) decreases ZEB1-mediated EMT and invasion by attenuation of IGF-1 receptor signaling in breast cancer

Early drug development of inhibitors of the insulin-like growth factor-I receptor pathway: lessons from the first clinical trials.

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4757-4772

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10.18632/ONCOTARGET.3023

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Ganji Purnachandra Nagaraju

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270282943

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4467113

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