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Oxidative Stress and Autophagy in Cancer Cells

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1414

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Guest Editor
Oral Ecology Research Group, Faculty of Dental Medicine, Laval University, Quebec, QC G1V 0A6, Canada
Interests: oral cancer

Special Issue Information

Dear Colleagues,

Oxidative stress is an important regulator in various pathways including apoptosis and autophagy. Much of the evidence indicates that autophagy and oxidative stress are both key, important contributors to tumorigenesis and cancer progression. Thus, a detailed study of the role of ROS and autophagy is needed to understand their role in cancer initiation and progression and to design effective therapies targeting redox regulation and autophagy systems for cancer therapy. Autophagy is a tumor suppressor pathway but can promote cancer cell survival under diverse stress conditions. Similarly, increased ROS has been implicated in tumorigenesis caused by diverse infectious or environmental agents as well as in the maintenance of cancer cell signaling pathways, but it has been suggested to limit metastasis formation. Various drugs, including phytochemicals and small molecules, are presently being investigated in preclinical and clinical studies that attribute their anticancer activity to ROS induction or to the induction of cell autophagy. Consistently, this Special Issue, “Oxidative Stress and Autophagy in Cancer Cells”, will cover a selection of recent research topics and current review articles in the field on the role of oxidative stress and autophagy processes in cancer progression.

Prof. Dr. Abdelhabib Semlali
Guest Editor

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Keywords

  • oxidative stress
  • autophagy
  • apoptosis
  • cancer cells
  • cancer cell signaling pathways

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Published Papers (1 paper)

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Research

23 pages, 11450 KiB  
Article
Inhibition Effects and Mechanism Study of rAj-HRP30, a Recombinant Histidine-Rich Peptide from Apostichopus japonicus, on the Viability of Pancreatic Ductal Adenocarcinoma Cells Panc01 and Panc02
by Yuyao Song, Shan Gao, Jingwei Jiang, Yuebin Zhang, Jingyu Zhang, Xiaona Wang, Li Lv, Zunchun Zhou and Jihong Wang
Int. J. Mol. Sci. 2025, 26(4), 1485; https://doi.org/10.3390/ijms26041485 - 11 Feb 2025
Viewed by 912
Abstract
rAj-HRP30 is a recombinant peptide derived from the wild-type rAj-HRP of Apostichopus japonicus through a gene-shortening mutation. It has a high histidine content (53.3% in its primary structure) and a molecular weight of 3.919 kDa, classifying it as a histidine-rich peptide. The literature [...] Read more.
rAj-HRP30 is a recombinant peptide derived from the wild-type rAj-HRP of Apostichopus japonicus through a gene-shortening mutation. It has a high histidine content (53.3% in its primary structure) and a molecular weight of 3.919 kDa, classifying it as a histidine-rich peptide. The literature reports indicate that human histidine-rich peptides exhibit antitumor activity. Previous research by our group demonstrated similar properties in rAj-HRP, the precursor of rAj-HRP30. Therefore, this study used Panc01 (human) and Panc02 (mouse) cells—highly malignant models with limited targeted therapies—to investigate the antitumor activity and mechanisms of rAj-HRP30 and evaluate its potential for pancreatic cancer treatment. This study designed a gene-shortening strategy for rAj-HRP and artificially synthesized the gene sequence of rAj-HRP30. The cDNA sequence of rAj-HRP30 was cloned into the pET23b vector, and the recombinant plasmid pET23b-HRP30 was transformed into E. coli BL21 for expression. Following IPTG induction, the recombinant peptide was purified using nickel ion affinity chromatography, yielding rAj-HRP30 with a purity exceeding 95%. rAj-HRP30 markedly inhibited the adhesion, migration, and invasion of Panc01 and Panc02 cells. It also disrupted cellular morphology and cytoskeletal structure while inducing apoptosis. These effects were dose-dependent. After confirming the in vitro anticancer activity of rAj-HRP30, this study employed Panc02 cells as a model to investigate its inhibitory mechanisms using Western blot analysis. The results revealed that rAj-HRP30 reduced FGFR1 expression in Panc02 cells and inhibited the downstream FYN and FAK signaling pathways, subsequently blocking the PI3K/AKT signaling and apoptosis pathways. In the apoptotic pathway, rAj-HRP30 was able to downregulate the expression of Bcl-2, Caspase-9, Caspase-3, Caspase-7, and PARP1 and upregulate the expression of Bax, cleaved Caspase-9, cleaved Caspase-3, cleaved Caspase-7, and cleaved-PARP1 to induce apoptosis in Panc02 cells. Furthermore, rAj-HRP30 also downregulated the expression of MMP2 and MMP9, thereby inhibiting the migration and invasion of Panc02 cells. Conclusion: rAj-HRP30 exhibits significant inhibitory effects on pancreatic ductal adenocarcinoma Panc01 and Panc02 cells in vitro. Its mechanism involves FGFR1-related signaling and apoptosis pathways. rAj-HRP30 shows promise as a therapeutic agent targeting FGFR for pancreatic cancer. Full article
(This article belongs to the Special Issue Oxidative Stress and Autophagy in Cancer Cells)
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