TRIM28 inhibits alternative lengthening of telomere phenotypes by protecting SETDB1 from degradation.

ABSTRACT:

Background

About 10-15% of tumor cells extend telomeres through the alternative lengthening of telomeres (ALT) mechanism, which is a recombination-dependent replication pathway. It is generally believed that ALT cells are related to the chromatin modification of telomeres. However, the mechanism of ALT needs to be further explored.

Results

Here we found that TRIM28/KAP1 is preferentially located on the telomeres of ALT cells and interacts with telomeric shelterin/telosome complex. Knocking down TRIM28 in ALT cells delayed cell growth, decreased the level of C-circle which is one kind of extrachromosomal circular telomeric DNA, increased the frequency of ALT-associated promyelocytic leukemia bodies (APBs), led to telomere prolongation and increased the telomere sister chromat

SUBMITTER: Wang C 

PROVIDER: S-EPMC8325274 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature