AI Article Synopsis
- Liver kinase B1 (LKB1) is a key enzyme linked to Peutz-Jeghers syndrome, which typically plays a role in protecting cancer cells from metabolic stress while promoting their survival and spread.
- This review highlights how LKB1's role in cancer contradicts the idea of it being a tumor suppressor, as its deletion leads to increased stress and genomic instability in cancer cells.
- The authors explore how mutated LKB1 works with other genes to help cancer cells adapt to harsh metabolic conditions, ultimately leading to more aggressive cancer behavior.
Article Abstract
Liver kinase B1 (LKB1) is an essential serine/threonine kinase frequently associated with Peutz-Jeghers syndrome (PJS). In this review, we provide an overview of the role of LKB1 in conferring protection to cancer cells against metabolic stress and promoting cancer cell survival and invasion. This carcinogenic effect contradicts the previous conclusion that LKB1 is a tumor suppressor gene. Here we try to explain the contradictory effect of LKB1 on cancer from a metabolic perspective. Upon deletion of LKB1, cancer cells experience increased energy as well as oxidative stress, thereby causing genomic instability. Meanwhile, mutated LKB1 cooperates with other metabolic regulatory genes to promote metabolic reprogramming that subsequently facilitates adaptation to strong metabolic stress, resulting in development of a more aggressive malignant phenotype. We aim to specifically discuss the contradictory role of LKB1 in cancer by reviewing the mechanism of LKB1 with an emphasis on metabolic stress and metabolic reprogramming.
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| http://dx.doi.org/10.1016/j.biopha.2020.110872 | DOI Listing |
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