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. Author manuscript; available in PMC: 2021 Aug 2.
Published in final edited form as: Oncogene. 2021 Feb 2;40(9):1690–1705. doi: 10.1038/s41388-021-01658-z

Fig 8. Working model depicting how AR-CAMKK2-AMPK signaling regulates autophagy by ULK1 phosphorylation and activation in prostate cancer.

Fig 8.

AR increases the expression of CAMKK2 which in turn phosphorylates and activates AMPK at threonine 172. As a result, AMPK phosphorylates ULK1 at serine 555 which activates the ULK1 complex and initiates autophagy in an mTOR-independent manner, supporting prostate cancer growth. This growth and survival mechanism can be blocked at several steps and as such, offers alternative strategies for targeting autophagy in prostate cancer.