Identification of nuclear export signal in KLLN suggests potential role in proteasomal degradation in cancer cells.

ABSTRACT: Germline and somatic promoter hypermethylation of KLLN has been found in diverse heritable and sporadic cancers, respectively. KLLN has many identified tumor suppressor functions, and when first reported, was thought to be exclusively nuclear. Here, we report on KLLN localization in both the nucleus and cytoplasm and the identification of a putative nuclear export signal (NES) sequence. KLLN overexpression in colon and breast cancer cells showed both nuclear and cytoplasmic presence. Inhibition of the CRM1 export pathway increased nuclear sequestration of KLLN, confirming the prediction of an NES sequence. Point mutations introduced in the predicted NES sequence decreased the strength of the NES and increased the nuclear sequestration of KLLN. Contrary to expectations, the transcrip

SUBMITTER: Sankunny M 

PROVIDER: S-EPMC7747863 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature