Effects of PRELI in oxidative-stressed HepG2 cells

Bo Yong Kim, Min Ho Cho, Kyung Joo Kim, Kyung Jin Cho, Suhng Wook Kim, Hyun Sook Kim, Woon Won Jung, Boo Hyung Lee, Bong Hee Lee, Seung Gwan Lee

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


Protein of relevant evolutionary and lymphoid interest (PRELI) is known for preventing apoptosis by mediating intramitochondrial transport of phosphatidic acid. However, the role of PRELI remains unclear. This study has demonstrated functions of PRELI through PRELI-knockdown in hepatocellular carcinoma (HepG2) cells exposed to oxidative stress by hydrogen peroxide. Results show that PRELI has three functions in HepG2 cells with regard to oxidative stress. First, PRELI affects expressional regulation of SOD-1 and caspase-3 genes in HepG2 cells. PRELI knockdown HepG2 cells have shown up-regulation of caspase-3 and down-regulation of SOD-1. Second, PRELI suppresses mitochondrial apoptosis in HepG2 cells. Fluorescence intensity related to mitochondrial apoptosis in PRELI-knockdown HepG2 cells increased more than two-fold compared to normal HepG2 cells. Third, PRELI suppresses senescence of HepG2 cells with oxidative stress. PRELI knockdown HepG2 cells showed higher levels of senescence than normal HepG2 cells. These results suggest that PRELI is a crucial protein in the suppression of apoptosis in HepG2 cells in response to oxidative stress.

Original languageEnglish
Pages (from-to)419-425
Number of pages7
JournalAnnals of Clinical and Laboratory Science
Issue number4
Publication statusPublished - 2015

Bibliographical note

Publisher Copyright:
© 2015 by the Association of Clinical Scientists, Inc.


  • HepG2 cell
  • Oxidative stress
  • Reactive oxygen species
  • Transfection
  • shRNA

ASJC Scopus subject areas

  • General Medicine


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