ArticleCancer science2025
A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Transcriptional activation of GSTP1 by ANXA3 is associated with cisplatin sensitivity in colorectal cancer cells.Oncology letters · 2026Article
- Association between the expression of GSTP1 and mutant p53, poor chemotherapy response and metastasis in patients with osteosarcoma.Oncology letters · 2026Article
- Genetic Modulation of Mercury Exposure on Perinatal and Birth Outcomes: A Systematic Review and Meta-Analysis of Gene-Environment Interactions.Journal of xenobiotics · 2026Review
- Mechanistic insights into hepatic metastasis of pancreatic cancer: molecular perspectives.Translational gastroenterology and hepatology · 2026Review
- CluVar: clustering of variants using autoencoder for inferring cancer subclones from single cell RNA sequencing data.Briefings in bioinformatics · 2025Article
- Oncogenic Role and Drug Resistance Effect of CCDC6 in iCCA: Potential Strategies for Targeted Intervention.Journal of cellular and molecular medicine · 2025Article
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11 authors.
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Abstract
Glutathione S-transferase P1 (GSTP1), a classic tumor biomarker, plays a controversial role in cancer progression. However, its specific role in pancreatic cancer (PC) has rarely been investigated. In the present study, we investigated the function and relationship between GSTP1 and mutant/wild-type p53 (mtp53/wtp53) in PC in vitro and in vivo. Compared with paired adjacent normal pancreas tissue, GSTP1 was downregulated in PC tissue, which was closely correlated with lymph node metastasis, Union for International Cancer Control (UICC) stage, and a better outcome of PC patients, processes dependent on wtp53 rather than mtp53. Moreover, a mutual regulation between GSTP1 and p53 was found in wtp53 PC cells. GSTP1 overexpression inhibited cell proliferation and chemotherapy resistance in vitro via wtp53/p21 and Bax/Bcl2 signaling, which was significantly reversed by wtp53 silencing, and vice versa. Similarly, the coordination of GSTP1 and p53 regulated the invasion and migration of PC cells, which was accompanied by changes in epithelial-mesenchymal transition (EMT) signaling (E-cad, ZO-1 and MMP9). Moreover, GSTP1 overexpression inhibited tumor growth and liver metastasis in vivo, as did high wtp53 and low ki67 expression. Interestingly, GSTP1 did not coimmunoprecipitate with either mtp53 or wtp53 in vitro. However, the wtp53 protein, as a transcription factor, could bind to the GSTP1 DNA promoter to transactivate GSTP1 mRNA expression as demonstrated via a Chip assay. Additionally, GSTP1 promoted the translocation of wtp53 into the nucleus but not mtp53. These results suggest that the positive feedback regulation of GSTP1 and wtp53 plays a significant role in cell proliferation, drug resistance, cell invasion and metastasis in PC.
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