Title:Analysis of the Expression of PRDX6 in Patients with Hepatocellular
Carcinoma and its Effect on the Phenotype of Hepatocellular Carcinoma
Cells
Volume: 25
Issue: 1
Author(s): Runhong Mu, Mingzhu Chang, Chuanbo Feng, Yunhe Cui, Tingyu Li, Chang Liu, Yilin Wang and Xiao Guo*
Affiliation:
- School of Pharmacy, Beihua University,
Jilin, 132000, P. R. China
Keywords:
Hepatocellular carcinoma (HCC), peroxiredoxin 6 (PRDX6), lentivirus, gene knockdown, phenotype, RNA sequence data.
Abstract:
Objectives: This research aimed to study the expression of PRDX6 mRNA in hepatocellular
carcinoma (HCC) and its effect on the prognosis of HCC. Moreover, the effect of PRDX6
gene knockdown on the proliferation, migration, and invasion of HepG2 cells mediated by lentivirus
was also examined. This study offers a theoretical and experimental basis for further research
on the mechanism of PRDX6 in liver cancer and new methods for clinical diagnosis and
treatment.
Methods: RNA sequence data of 369 HCC patients were screened through the TCGA database,
and the expression and clinical characteristics of PRDX6 mRNA were analyzed based on high-
-throughput RNA sequencing data. HepG2 cells were divided into WT, sh-NC and sh-PRDX6
groups. Real-time PCR and Western blot were used to detect the expression levels of the PRDX6
gene and protein, respectively. CCK8 method was used to detect the proliferation activity of Hep-
G2 cells, scratch healing test was used to detect the migration ability, Transwell chamber was
used to detect the invasion ability, and Western blot was used to detect the expression levels of
PI3K/Akt/mTOR signaling pathway and Notch signaling pathway-related proteins.
Results: The expression of PRDX6 was significantly correlated with the gender, race, clinical
stage, histological grade, and survival time of HCC patients (P < 0.05). Compared with that in
WT and sh-NC groups, the expression level of PRDX6 protein in HCC patients was significantly
lower (P < 0.01), the proliferation activity of HCC cells was significantly decreased (P < 0.05),
and the migration and invasion ability was significantly decreased (P < 0.05) in the sh-PRDX6
group. The expression levels of PI3K, p-Akt, p-mTOR, Notch1, and Hes1 proteins in the sh-
PRDX6 group were significantly lower than those in WT and sh-NC groups (P < 0.05).
Conclusion: The expression of PRDX6 may be closely related to the prognosis of HCC. Lentivirus-
mediated PRDX6 knockdown can inhibit the proliferation, migration and invasion of HCC
cells, which may be related to its regulating the PI3K/Akt/mTOR and Notch1 signaling pathways.
PRDX6 is expected to be a new target for the diagnosis and treatment of liver cancer.
