Role of HER‐2/neu signaling in sensitivity to tumor necrosis factor‐related apoptosis‐inducing ligand: Enhancement of TRAIL‐mediated apoptosis by amiloride
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Summary
It is suggested that amiloride enhances TRAIL‐induced cytotoxicity by inhibiting phosphorylation of the HER‐2/neu‐PI3K‐Akt pathway‐associated kinases and phosphatase.
- Type
- article
- Published
- 2005-10-01
- Cited by
- 12
- References
- 68
- OpenAlex
- https://openalex.org/W1966392199
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:42896310
Keywords
Amiloride, Cancer research, Protein kinase B, Apoptosis, PI3K/AKT/mTOR pathway
References
- Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery.
- PTEN sensitizes prostate cancer cells to death receptor-mediated and drug-induced apoptosis through a FADD-dependent pathway
- Amiloride directly inhibits growth factor receptor tyrosine kinase activity.
- Tumoricidal activity of tumor necrosis factor–related apoptosis–inducing ligand in vivo
- How TRAIL Kills Cancer Cells, But Not Normal Cells
- TRAIL receptor-2 signals apoptosis through FADD and caspase-8
- Involvement of tumor necrosis factor-related apoptosis-inducing ligand in surveillance of tumor metastasis by liver natural killer cells
- Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand
- Effects of amiloride on thermosensitivity of Chinese hamster cells under neutral and acidic pH.
- p53-dependent and -independent regulation of the death receptor KILLER/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alpha.
- NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase
- Evidence that a Na+/Ca2+ antiport system regulates murine erythroleukemia cell differentiation.
- Activation of phosphoinositide 3‐kinase by interaction with Ras and by point mutation.
- CFTR modulates programmed cell death by decreasing intracellular pH in Chinese hamster lung fibroblasts.
- The heat shock protein 90 inhibitor geldanamycin and the ErbB inhibitor ZD1839 promote rapid PP1 phosphatase-dependent inactivation of AKT in ErbB2 overexpressing breast cancer cells.
- Role of glycogen synthase kinase-3beta in neuronal apoptosis induced by trophic withdrawal.
- Caspases: the executioners of apoptosis.
- IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs.
- Three-dimensional structure of the catalytic subunit of protein serine/threonine phosphatase-1
- Combined effect of tumor necrosis factor-related apoptosis-inducing ligand and ionizing radiation in breast cancer therapy.
Cited by
- Synthesis and biological evaluation of plasminogen activation inhibitors as antitumour/antimetastasis agents
- Why are breast cancer stem cells resistant to radiation
- Enhancement of cytotoxic and pro-apoptotic effects of 2-aminophenoxazine-3-one on the rat hepatocellular carcinoma cell line dRLh-84, the human hepatocellular carcinoma cell line HepG2, and the rat normal hepatocellular cell line RLN-10 in combination with 2-deoxy-D-glucose.
- Overcoming TRAIL resistance in ovarian carcinoma.
- 2-Aminophenoxazine-3-one and 2-amino-4,4α-dihydro-4α,7-dimethyl-3H-phenoxazine-3-one cause cellular apoptosis by reducing higher intracellular pH in cancer cells
- ERBB1/EGFR and ERBB2 (HER2/neu)--targeted therapies in cancer and cardiovascular system with cardiovascular drugs.
- Anti‐tumour/metastasis effects of the potassium‐sparing diuretic amiloride: An orally active anti‐cancer drug waiting for its call‐of‐duty?
- Phenylbenzopyrones structure-activity studies identify betuletol derivatives as potential antitumoral agents.
- Multifaceted targeting in cancer: the recent cell death players meet the usual oncogene suspects
- The inhibition of Bid expression by Akt leads to resistance to TRAIL-induced apoptosis in ovarian cancer cells
- Integrating immune cell functions and apoptosis-based therapies for the treatment of ovarian cancer
- Amiloride synergizes with EGFR PROTACs and inhibitors to overcome therapeutic resistance in NSCLC.
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