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Cited by 242

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy

Open access
Lister, Adam, Nedjadi, Taoufik, Kitteringham, Neil R, Campbell, Fiona, Costello, Eithne, Lloyd, Bryony, Copple, Ian M, Williams, Samantha, Owen, Andrew, Neoptolemos, John P, Goldring, Chris E, Park, B Kevin·2011·Molecular Cancer
DOI 10.1186/1476-4598-10-37
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Abstract

Background: Nrf2 is a key transcriptional regulator of a battery of genes that facilitate phase II/III drug metabolism and defence against oxidative stress. Nrf2 is largely regulated by Keap1, which directs Nrf2 for proteasomal degradation. The Nrf2/Keap1 system is dysregulated in lung, head and neck, and breast cancers and this affects cellular proliferation and response to therapy. Here, we have investigated the integrity of the Nrf2/Keap1 system in pancreatic cancer. Results: Keap1, Nrf2 and the Nrf2 target genes AKR1c1 and GCLC were detected in a panel of five pancreatic cancer cell lines. Mutation analysis of NRF2 exon 2 and KEAP1 exons 2-6 in these cell lines identified no mutations in NRF2 and only synonomous mutations in KEAP1. RNAi depletion of Nrf2 caused a decrease in the proliferation of Suit-2, MiaPaca-2 and FAMPAC cells and enhanced sensitivity to gemcitabine (Suit-2), 5-flurouracil (FAMPAC), cisplatin (Suit-2 and FAMPAC) and gamma radiation (Suit-2). The expression of Nrf2 and Keap1 was also analysed in pancreatic ductal adenocarcinomas (n = 66 and 57, respectively) and matching normal benign epithelium (n = 21 cases). Whilst no significant correlation was seen between the expression levels of Keap1 and Nrf2 in the tumors, interestingly, Nrf2 staining was significantly greater in the cytoplasm of tumors compared to benign ducts (P < 0.001). Conclusions: Expression of Nrf2 is up-regulated in pancreatic cancer cell lines and ductal adenocarcinomas. This may reflect a greater intrinsic capacity of these cells to respond to stress signals and resist chemotherapeutic interventions. Nrf2 also appears to support proliferation in certain pancreatic adenocarinomas. Therefore, strategies to pharmacologically manipulate the levels and/or activity of Nrf2 may have the potential to reduce pancreatic tumor growth, and increase sensitivity to therapeutics.

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Metadata

Authors
Lister, A., Nedjadi, T., Kitteringham, N. R., Campbell, F., Costello, E., Lloyd, B., Copple, I. M., Williams, S., Owen, A., Neoptolemos, J. P., Goldring, C. E., & Park, B. K.
Venue
Molecular Cancer
Publisher
Springer Science and Business Media LLC
Published
2011-04-13
Volume
10
Issue
1
Pages
37-37
ISSN
1476-4598 (ISSN-L)
DOI
10.1186/1476-4598-10-37
OpenAlex
W2137862511
Cited by
242
References
7
FWCI
5.76
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy. https://app.cochat.ai/papers/10.1186/1476-4598-10-37
The paper
Lister, A., Nedjadi, T., Kitteringham, N. R., Campbell, F., Costello, E., Lloyd, B., Copple, I. M., Williams, S., Owen, A., Neoptolemos, J. P., Goldring, C. E., & Park, B. K. (2011). Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy. Molecular Cancer. https://doi.org/10.1186/1476-4598-10-37

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.