The SIRT2-mediated deacetylation of AKR1C1 is required for suppressing its pro-metastasis function in Non-Small Cell Lung Cancer.

ABSTRACT: Aldo-keto reductase family 1 member C1 (AKR1C1) promotes malignancy of Non-Small Cell Lung Cancer (NSCLC) by activating Signal Transducer and Activator of Transcription 3 (STAT3) pathway. However, how the pro-metastatic functions of AKR1C1 are switched on/off remains unknown. Methods: Immunoprecipitation and LC-MS/MS analyses were performed to identify the acetylation on AKR1C1 protein, and the functional analyses (in vitro and in vivo) were performed to depict the contribution of acetylation to the pro-metastatic effects of AKR1C1. Results: Here we report that acetylated AKR1C1 on two lysine residues K185 & K201 is critical to its pro-metastatic role. The acetylation modification has no impact on the canonical enzymatic activity of AKR1C1, while it is required

SUBMITTER: Zhu H 

PROVIDER: S-EPMC7019158 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature