ArticleInternational journal of clinical and experimental pathology2018
Graphene oxide regulates endoplasmic reticulum stress: autophagic pathways in nasopharyngeal carcinoma cells.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Autophagy-modulating biomaterials: multifunctional weapons to promote tissue regeneration.Cell communication and signaling : CCS · 2024Review
- Autophagy-mediated nanomaterials for tumor therapy.Frontiers in oncology · 2023Review
- Graphene Oxide Enhances Biogenesis and Release of Exosomes in Human Ovarian Cancer Cells.International journal of nanomedicine · 2022Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
During carcinogenesis, growth, proliferation, invasion and metastasis, increasing evidence shows that autophagy and endoplasmic reticulum stress (ER stress) are regulated in nasopharyngeal carcinoma, a finding drawing more attention from physicians and scientists. As one of the carbon-based nano-materials, graphene oxide (GO) has been extensively used for its advantages, such as biocompatibility, an ultrahigh surface to volume ratio, abundant surface groups, and a special photothermal effect. The present study is designed to explore the effects of GO on autophagy and ER stress in nasopharyngeal carcinoma cells. Our findings will provide scientific bases for the clinical application of GO and the development of new analogues. GO inhibits the proliferation of HONE1 cells, promotes their apoptosis in a concentration-dependent manner and enhances the expression of the ER stress chaperone GRP78 in HONE1 cells. These results suggest that GO could affect HONE1 cells through the autophagic and ER stress pathways. Thus, GO inhibits the proliferation of nasopharyngeal carcinoma cells via the induction of cytotoxic autophagy. In addition, ER stress is also activated as an adaptive response, so blocking ER stress may enhance the sensitivity of nasopharyngeal carcinoma cells to GO.
Indexed as
Identifiers
31949666PMC6963062W3012357267What OpenQuestion holds
Registered trials
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