ArticleExperimental and therapeutic medicine2024
GPX3 represses pancreatic cancer cell proliferation, migration and invasion, and improves their chemo‑sensitivity by regulating the JNK/c‑Jun signaling pathway.
Article in Experimental and therapeutic medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Asynchronous Evolution of Epithelium and Stroma Differentiates Precursor Lesions from Pancreatic Cancer.Cancer discovery · 2026Article
- Ferroptosis-Based Nanotherapy for Pancreatic Ductal Adenocarcinoma Through Glutathione Depletion and Iron Accumulation.International journal of nanomedicine · 2026Review
- Identification of GPX3 and JUN as Tumor Suppressors in Thyroid Cancer through Integrated WGCNA and Mendelian Randomization.Journal of Cancer · 2025Article
- Glutathione-Dependent Pathways in Cancer Cells.International journal of molecular sciences · 2024Review
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer (PC) is a deadly and aggressive disease, which is characterized by poor prognosis. It has been reported that glutathione peroxidase 3 (GPX3) is involved in the development of several types of cancer. The present study aimed to explore the regulatory role of GPX3 in PC and uncover its underlying mechanism. Bioinformatics analysis was initially carried out to predict the expression profile of GPX3 in PC and its association with prognosis. The expression levels of GPX3 were also detected in PC cells by reverse transcription-quantitative PCR and western blot analysis. Following transfection to induce GPX3 overexpression, the proliferation ability of PC cells was assessed by Cell Counting Kit-8, colony formation and 5-ethynyl-2'-deoxyuridine incorporation assays. In addition, wound healing and Transwell assays were performed to evaluate the migration and invasion abilities of PC cells. Cell apoptosis was assessed by flow cytometric analysis. The expression levels of epithelial-mesenchymal transition (EMT)-, apoptosis-, and JNK signaling-related proteins were detected by western blot analysis. Additionally, for rescue experiments, JNK signaling was activated following cell treatment with anisomycin. The results showed that GPX3 was downregulated in PC and its expression was associated with favorable prognosis. In addition, cell transfection-induced GPX3 overexpression markedly inhibited cell proliferation, migration and invasion, and inhibited EMT. In addition, GPX3 improved the chemo-sensitivity of PC and gemcitabine (GEM)-resistant PC cells to GEM. Furthermore, GPX3 significantly suppressed JNK/c-Jun signaling in PC, while anisomycin treatment reversed the inhibitory effects of GPX3 on the malignant behavior and chemo-resistance of PC cells. The results of the present study indicated that GPX3 could serve as a tumor suppressor in PC via inhibiting JNK/c-Jun signaling, thus providing novel insights into the treatment of PC.
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