A cis-eQTL genetic variant in PLK4 confers high risk of hepatocellular carcinoma.

ABSTRACT:

Purpose

The overexpression and knockdown of PLK4 were both reported to generate aneuploidy. Thus, we aimed to investigate whether genetic variants in PLK4 contribute to the development of hepatocellular carcinoma (HCC).

Methods

We evaluated associations of common variants in PLK4 and its promoter for the risk of HCC in our association study (1300 cases and 1344 controls). The genotype-tissue expression (GTEx) and The cancer genome atlas (TCGA) databases were used to quantify the expression of PLK4. Cell proliferation and migration affected by PLK4 in HCC were assessed in vitro. Drug susceptibility testing (DST) model was used to assess the sensibility of PLK4-activated HCC to CFI-400945, a small molecule inhibitor of PLK4.

Results

Herein, we found a significant associ

SUBMITTER: Meng L 

PROVIDER: S-EPMC6797585 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature