Interleukin 6 alters localization of hMSH3, leading to DNA mismatch repair defects in colorectal cancer cells.

ABSTRACT:

Background & aims

Elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) is the most common DNA mismatch repair defect in colorectal cancers, observed in approximately 60% of specimens. This acquired genotype correlates with metastasis and poor outcomes for patients, and is associated with intra-epithelial inflammation and heterogeneous nuclear levels of the mismatch repair protein hMSH3. Inflammation and accompanying oxidative stress can cause hMSH3 to change its intracellular location, but little is known about the source of oxidative stress in cancer cells. We investigated whether cytokines mediate this process.

Methods

We analyzed levels of interleukin 6 (IL6) and its receptor (IL6R) in human colon and lung cancer cell lines by flow cytometry and

SUBMITTER: Tseng-Rogenski SS 

PROVIDER: S-EPMC4339542 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature