The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms

Recombinant human peroxiredoxin-5 (hPRDX5), isolated from anti-cancer bioactive peptide (ACBPs), shows a homology of 89% with goat peroxiredoxin-5 (gPRDX5) and is reported to display anti-tumor activity in vivo. Herein, we explored the effect of hPRDX5 and the responsible mechanism in treating pancr...

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Main Authors: Lihua Cui, Yuanyuan Jin, Sen Zou, Jing Xun, Xiangyang Yu, Qi Zhang, Zhaoyong Yang
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 2022-09-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2022000100658&tlng=en
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author Lihua Cui
Yuanyuan Jin
Sen Zou
Jing Xun
Xiangyang Yu
Qi Zhang
Zhaoyong Yang
author_facet Lihua Cui
Yuanyuan Jin
Sen Zou
Jing Xun
Xiangyang Yu
Qi Zhang
Zhaoyong Yang
author_sort Lihua Cui
collection DOAJ
description Recombinant human peroxiredoxin-5 (hPRDX5), isolated from anti-cancer bioactive peptide (ACBPs), shows a homology of 89% with goat peroxiredoxin-5 (gPRDX5) and is reported to display anti-tumor activity in vivo. Herein, we explored the effect of hPRDX5 and the responsible mechanism in treating pancreatic cancer. Tumor-bearing mice were randomly divided into normal PBS group and treatment group (n=5; 10 mg/kg hPRDX5). Flow cytometry was employed to examine lymphocytes, myeloid-derived suppressor cell subsets, and the function proteins of natural killer (NK) cells in peripheral blood, spleen, and tumor tissues of mice. Western blot was used to measure the protein expressions of the key nodes in TLR4-MAPK-NF-κB signaling pathway. The rate of tumor suppression was 57.6% at a 10 mg/kg dose in orthotopic transplanted tumor mice. Moreover, the population of CD3+CD4+T cells, NK cells, and CD3+CD8+T cells was significantly increased in the tumor tissue of the hPRDX5 group, while the proportion of granulocytic-myeloid-derived suppressor cells decreased slightly. In addition, after treatment with hPRDX5, the percentage of NK cells in blood increased more than 4-fold. Our findings indicated that hPRDX5 effectively suppressed pancreatic cancer possibly via the TLR4-MAPK-NF-κB signaling cascade; hence hPRDX5 could be a prospective immunotherapy candidate for treating pancreatic cancer.
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spelling doaj.art-be13ba6840f34c78b448c0b383515b2a2022-12-22T03:47:35ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research1414-431X2022-09-015510.1590/1414-431x2022e12324The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanismsLihua Cuihttps://orcid.org/0000-0002-7921-4225Yuanyuan Jinhttps://orcid.org/0000-0002-1284-9736Sen Zouhttps://orcid.org/0000-0002-6593-0618Jing Xunhttps://orcid.org/0000-0002-8730-4212Xiangyang Yuhttps://orcid.org/0000-0002-3688-347XQi Zhanghttps://orcid.org/0000-0002-7817-2211Zhaoyong Yanghttps://orcid.org/0000-0001-7197-3991Recombinant human peroxiredoxin-5 (hPRDX5), isolated from anti-cancer bioactive peptide (ACBPs), shows a homology of 89% with goat peroxiredoxin-5 (gPRDX5) and is reported to display anti-tumor activity in vivo. Herein, we explored the effect of hPRDX5 and the responsible mechanism in treating pancreatic cancer. Tumor-bearing mice were randomly divided into normal PBS group and treatment group (n=5; 10 mg/kg hPRDX5). Flow cytometry was employed to examine lymphocytes, myeloid-derived suppressor cell subsets, and the function proteins of natural killer (NK) cells in peripheral blood, spleen, and tumor tissues of mice. Western blot was used to measure the protein expressions of the key nodes in TLR4-MAPK-NF-κB signaling pathway. The rate of tumor suppression was 57.6% at a 10 mg/kg dose in orthotopic transplanted tumor mice. Moreover, the population of CD3+CD4+T cells, NK cells, and CD3+CD8+T cells was significantly increased in the tumor tissue of the hPRDX5 group, while the proportion of granulocytic-myeloid-derived suppressor cells decreased slightly. In addition, after treatment with hPRDX5, the percentage of NK cells in blood increased more than 4-fold. Our findings indicated that hPRDX5 effectively suppressed pancreatic cancer possibly via the TLR4-MAPK-NF-κB signaling cascade; hence hPRDX5 could be a prospective immunotherapy candidate for treating pancreatic cancer.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2022000100658&tlng=enRecombinant human peroxiredoxin-5Pancreatic cancerImmunotherapyImmune cells activationMyeloid-derived suppressor cells
spellingShingle Lihua Cui
Yuanyuan Jin
Sen Zou
Jing Xun
Xiangyang Yu
Qi Zhang
Zhaoyong Yang
The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
Brazilian Journal of Medical and Biological Research
Recombinant human peroxiredoxin-5
Pancreatic cancer
Immunotherapy
Immune cells activation
Myeloid-derived suppressor cells
title The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
title_full The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
title_fullStr The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
title_full_unstemmed The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
title_short The antitumor activity of hPRDX5 against pancreatic cancer and the possible mechanisms
title_sort antitumor activity of hprdx5 against pancreatic cancer and the possible mechanisms
topic Recombinant human peroxiredoxin-5
Pancreatic cancer
Immunotherapy
Immune cells activation
Myeloid-derived suppressor cells
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2022000100658&tlng=en
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