内质网
未折叠蛋白反应
ATF6
前列腺癌
医学
串扰
癌症研究
癌变
雄激素受体
转移
前列腺
癌症
细胞生物学
生物
内科学
光学
物理
作者
Claire M. de la Calle,Kevin Shee,Heiko Yang,Peter E. Lonergan,Hao G. Nguyen
标识
DOI:10.1038/s41585-022-00649-3
摘要
In order to proliferate in unfavourable conditions, cancer cells can take advantage of the naturally occurring endoplasmic reticulum-associated unfolded protein response (UPR) via three highly conserved signalling arms: IRE1α, PERK and ATF6. All three arms of the UPR have key roles in every step of tumour progression: from cancer initiation to tumour growth, invasion, metastasis and resistance to therapy. At present, no cure for metastatic prostate cancer exists, as targeting the androgen receptor eventually results in treatment resistance. New research has uncovered an important role for the UPR in prostate cancer tumorigenesis and crosstalk between the UPR and androgen receptor signalling pathways. With an improved understanding of the mechanisms by which cancer cells exploit the endoplasmic reticulum stress response, targetable points of vulnerability can be uncovered.
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