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Park, Chan Young
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Molecular interactions of autophagy with the immune system and cancer

Author(s)
Jin, YunhoHong, YunkyungPark, Chan YoungHong, Yonggeun
Issued Date
2017-08
DOI
10.3390/ijms18081694
URI
https://scholarworks.unist.ac.kr/handle/201301/22617
Fulltext
http://www.mdpi.com/1422-0067/18/8/1694
Citation
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.18, no.8, pp.1694
Abstract
Autophagy is a highly conserved catabolic mechanism that mediates the degradation of damaged cellular components by inducing their fusion with lysosomes. This process provides cells with an alternative source of energy for the synthesis of new proteins and the maintenance of metabolic homeostasis in stressful environments. Autophagy protects against cancer by mediating both innate and adaptive immune responses. Innate immune receptors and lymphocytes (T and B) are modulated by autophagy, which represent innate and adaptive immune responses, respectively. Numerous studies have demonstrated beneficial roles for autophagy induction as well as its suppression of cancer cells. Autophagy may induce either survival or death depending on the cell/tissue type. Radiation therapy is commonly used to treat cancer by inducing autophagy in human cancer cell lines. Additionally, melatonin appears to affect cancer cell death by regulating programmed cell death. In this review, we summarize the current understanding of autophagy and its regulation in cancer.
Publisher
MDPI AG
ISSN
1422-0067
Keyword (Author)
AutophagyCancerCell deathImmune systemMetabolic homeostasis
Keyword
DOUBLE-EDGED-SWORDTOLL-LIKE RECEPTORSCHAPERONE-MEDIATED AUTOPHAGYT-CELL HOMEOSTASISCOLORECTAL-CANCERINNATE IMMUNITYTHERAPYTUMORGENEMACROAUTOPHAGY

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