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S-Nitrosylation in Cancer Cells: To Prevent or to Cause?

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Abstract

The purpose of this review is to point out some important proteins targeted by chemotherapy in cancer patients as well as by NO (S-nitrosylation) in tumor cells. We, therefore, confronted data from clinical and preclinical studies and discussed their respective anti-tumor effects to determine whether the associations of chemotherapy with NO donor therapy may be considered as novel therapeutic approaches (considered as rational therapeutic interventions).

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Abbreviations

AR:

Androgen receptor

CCL4:

(C-C motif) ligand 4

DETANO:

Diethylenetriamine/nitric oxide

EGF:

Epidermal growth factor

EGFR:

Epidermal growth factor receptor

ERK:

Extracellular signal-regulated kinase

Fas (APO-1, CD95):

Apoptosis antigen 1

GSNO:

S-nitrosoglutatione

GTN:

Glyceryltrinitrate

HER:

Human epidermal growth factor receptor

HSP:

Heat shock protein

IAP:

Inhibitor of apoptosis protein

IKK:

IκB kinase

JNK:

c-jun NH2-terminal kinase

N2O3 :

Nitrogen trioxide

NF-κB:

Nuclear factor-kappa B

NO:

Nitric oxide

NO2 :

Nitrites

NO-NSAIDs:

NO-donating non-steroidal anti-inflammatory drugs

PKB:

Protein kinase B

PTEN:

Phosphatase and TENsin homolog

SM:

Smac mimetic

SNO:

S-nitrosothiol

STAT3:

Signal transduction and activator of transcription 3

TKI:

Tyrosine kinase inhibitor

TRAIL:

Tumor-necrosis-factor related apoptosis inducing ligand

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Bettaieb, A., Plenchette, S., Paul, C., Laurens, V., Romagny, S., Jeannin, JF. (2015). S-Nitrosylation in Cancer Cells: To Prevent or to Cause?. In: Bonavida, B. (eds) Nitric Oxide and Cancer: Pathogenesis and Therapy. Springer, Cham. https://doi.org/10.1007/978-3-319-13611-0_7

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