Role of GS28 in sodium nitroprusside‐induced cell death in cervical carcinoma cells
| Autor: | Oh-Joo Kwon, Jeong-Hwa Lee, Do Eun Rim, Seong-Whan Jeong, Hyung Jae Yoo |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Nitroprusside
0301 basic medicine MAPK/ERK pathway Programmed cell death Receptor complex NF-E2-Related Factor 2 Health Toxicology and Mutagenesis Uterine Cervical Neoplasms Toxicology Biochemistry HeLa 03 medical and health sciences symbols.namesake 0302 clinical medicine Autophagy Humans Phosphorylation Extracellular Signal-Regulated MAP Kinases Cytotoxicity Protein Kinase Inhibitors Molecular Biology Cell Death 030102 biochemistry & molecular biology biology Chemistry Golgi vesicle transport General Medicine Qb-SNARE Proteins Golgi apparatus biology.organism_classification Molecular biology 030220 oncology & carcinogenesis symbols Molecular Medicine Female Reactive Oxygen Species HeLa Cells |
| Zdroj: | Journal of Biochemical and Molecular Toxicology. 33 |
| ISSN: | 1099-0461 1095-6670 |
| Popis: | Golgi S-nitro-N-acetylpenicillamine receptor complex 1 (GS28) has been implicated in Golgi vesicle transport. We examined the role of GS28 and its molecular mechanisms in sodium nitroprusside (SNP)-induced cell death using GS28 siRNA (siGS28)-transfected HeLa cells. Significant inhibition of cytotoxicity was observed in the cells treated with SNP, and photodegraded SNP showed equal cytotoxicity to SNP. Pretreatment with an ERK inhibitor or siErk1 cotransfection blocked the inhibition in cytotoxicity. Additionally, increased phosphorylation of ERK was maintained in the cells treated with SNP, and Nrf2 level was dependent on ERK phosphorylation. However, pretreatment with a pan-caspase inhibitor had no effect on cytotoxicity or procaspase-3 level. Pretreatment with an autophagy inhibitor or siATG5 cotransfection blocked the inhibition of cytotoxicity. The changes of LC3 corresponded to that in siErk1-cotransfected cells. These data suggest that GS28 has an inductive role in SNP-induced cell death via inhibition of ERK, leading to inhibition of autophagic processes in HeLa cells. |
| Databáze: | OpenAIRE |
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