Alterations in the glycome after HDAC inhibition impact oncogenic potential in epigenetically plastic SW13 cells.

ABSTRACT:

Background

Defects in the type and degree of cellular glycosylation impact oncogenesis on multiple levels. Although the type of glycosylation is determined by protein sequence encoded by the genome, the extent and modifications of glycosylation depends on the activity of biosynthetic enzymes and recent data suggests that the glycome is also subject to epigenetic regulation. This study focuses on the ability of HDAC inhibition to alter glycosylation and to lead to pro-oncogenic alterations in the glycome as assessed by metastatic potential and chemoresistance.

Methods

Epigenetically plastic SW13 adrenocortical carcinoma cells were treated with FK228, an HDAC inhibitor with high affinity for HDAC1 and, to a lesser extent, HDAC2. In comparing HDAC inhibitor treated and control

SUBMITTER: Montgomery MR 

PROVIDER: S-EPMC6335691 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature