RCC2 over-expression in tumor cells alters apoptosis and drug sensitivity by regulating Rac1 activation.

ABSTRACT:

Background

Small GTP binding protein Rac1 is a component of NADPH oxidases and is essential for superoxide-induced cell death. Rac1 is activated by guanine nucleotide exchange factors (GEFs), and this activation can be blocked by regulator of chromosome condensation 2 (RCC2), which binds the switch regions of Rac1 to prevent access from GEFs.

Methods

Three cancer cell lines with up- or down-regulation of RCC2 were used to evaluate cell proliferation, apoptosis, Rac1 signaling and sensitivity to a group of nine chemotherapeutic drugs. RCC2 expression in lung cancer and ovarian cancer were studied using immunochemistry stain of tumor tissue arrays.

Results

Forced RCC2 expression in tumor cells blocked spontaneous- or Staurosporine (STS)-induced apoptosis. In contrast, R

SUBMITTER: Wu N 

PROVIDER: S-EPMC5763756 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature