Adriamycin activates c-jun N-terminal kinase in human leukemia cells: a relevance to apoptosis
References (35)
Cell surface actions of adriamycin
Pharmacol. Ther.
(1991)- et al.
How MAP kinases are regulated
J. Biol. Chem.
(1995) The mitogen-activated protein kinase signal transduction pathway
J. Biol. Chem.
(1993)- et al.
The small GTP-binding proteins Rac 1 and Cdc42 regulate the activity of the JNK/SAPK signaling pathway
Cell
(1995) - et al.
Selective activation of the JNK signaling cascade and c-jun transcriptional activity by the small GTPases Rac and Cdc42Hs
Cell.
(1995) The regulation of AP-1 activity by mitogen-activated protein kinases
J. Biol. Chem.
(1995)- et al.
ATF3 gene: genomic organization, promoter and regulation
J. Biol. Chem.
(1996) - et al.
JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain
Cell
(1994) - et al.
Persistent activation of c-Jun N-terminal kinase 1 (JNK1) in γ-radiation-induced apoptosis
J. Biol. Chem.
(1996) - et al.
Parallel signal processing among mammalian MAPKs
Trends Biochem. Sci.
(1995)
Activation of mitogen-activated protein kinase by H2O2: role in cell survival following oxidant injury
J. Biol. Chem.
Ceramide synthase mediates daunorubicin-induced apoptosis: an alternative mechanism for generating death signals
Cell
The biochemical basis of anthracycline toxicity and antitumor action
Rev. Biochem Toxicol.
The molecular basis for the action of some DNA-binding drugs
Prog. Med. Chem.
Adriamycin-induced DNA damage mediated by mammalian DNA topoisomerase II
Science
DNA topoisomerase poisons as antitumor drugs
Annu. Rev. Biochem.
NADPH cytochrome P-450 reductase activation of quinone anticancer agents to free radicals
Cited by (108)
Fangchinoline derivatives induce cell cycle arrest and apoptosis in human leukemia cell lines via suppression of the PI3K/AKT and MAPK signaling pathway
2020, European Journal of Medicinal ChemistryCitation Excerpt :The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway is associated with cell proliferation, differentiation, migration, aging and apoptosis [9]. In numerous studies, inhibition of ERK and JNK efficiently promoted apoptosis of leukemia cells, indicating their therapeutic benefit for this malignancy [10]. The above observations also suggest that dual inhibition of PI3K and MAPK pathway could produce an additive anti-cancer effect in AML cells.
Ampelopsin induces apoptosis in HepG2 human hepatoma cell line through extrinsic and intrinsic pathways: Involvement of P38 and ERK
2015, Environmental Toxicology and PharmacologyCitation Excerpt :Therefore, apoptosis-inducing agents are expected to be ideal anticancer drugs (Johnstone et al., 2002). Many therapeutic agents for cancer, such as cisplatin (Zhang et al., 2015), paclitaxel (Kumar et al., 2015), isothiocyanate (Chen et al., 1998), and adriamycin (Yu et al., 1996), had been reported to inhibit cancer cell growth through initiating apoptotic process. In addition, some flavonoids, such as quercetin, apigenin, and phloretin, also eliminate tumor cells by inducing apoptotic cell death (Wang et al., 1999).
Oxidative stress in the pathogenesis of psoriasis
2009, Free Radical Biology and MedicineThe Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses
2024, International Journal of Molecular Sciences
- 1
Contributed equally to this work.