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Cited by 338Endoplasmic Reticulum Stress and DiseaseHeat shock proteins researchCell death mechanisms and regulation

The DOI matches its Crossref record; 64 of the 65 references it cites were found in a registry or an index.

Overexpression of the glucose-regulated stress gene GRP78 in malignant but not benign human breast lesions

Fernandez, Patricia M., Tabbara, Sana O., Jacobs, Lisa K., Manning, Frank C. R., Tsangaris, Theodore N., Schwartz, Arnold M., Kennedy, Katherine A., Patierno, Steven R.·2000·Breast Cancer Research and Treatment
DOI 10.1023/a:1006332011207
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Abstract

The 78 kDa glucose-regulated stress protein GRP78 is induced by physiological stress conditions such as hypoxia, low pH, and glucose deprivation which often exist in the microenvironments of solid tumors. Activation of this stress pathway occurs in response to several pro-apoptotic stimuli. In vitro studies have demonstrated a correlation between induced expression of GRP78 and resistance to apoptotic death induced by topoisomerase II-directed drugs. We were interested in characterizing this protein in human breast lesions for potential implications in chemotherapeutic intervention. Surgical specimens of human breast lesions and paired normal tissues from the same patients were flash frozen for these studies. Total RNA and/or protein were extracted from these tissues and used in northern and/or western blot analyses, respectively, to quantify the relative expression of GRP78. Northern blot analysis indicated that 0/5 benign breast lesions, 3/5 estrogen receptor positive (ER+) breast tumors, and 6/9 estrogen receptor negative (ER-) breast tumors exhibited overexpression of GRP78 mRNA compared to paired normal tissues, with fold overexpressions ranging from 1.8 to 20. Western blot analyses correlated with these findings since 0/5 benign breast lesions, 4/6 ER+ breast tumors, and 3/3 ER- breast tumors overexpressed GRP78 protein with fold overexpressions ranging from 1.8 to 19. Immunohistochemical analysis of these tissues demonstrated that the expression of GRP78 was heterogeneous among the cells comprising different normal and malignant glands, but confirmed the overexpression of GRP78 in most of the more aggressive ER- tumors. These results suggest that some breast tumors exhibit adverse microenvironment conditions that induce the overexpression of specific stress genes that may play a role in resistance to apoptosis and decreased chemotherapeutic efficacy.

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Crossref · 10.1023/a:1006332011207

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64 of 64 references verified0 citation errors · 0 not checkable

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Metadata

Authors
Fernandez, P. M., Tabbara, S. O., Jacobs, L. K., Manning, F. C. R., Tsangaris, T. N., Schwartz, A. M., Kennedy, K. A., & Patierno, S. R.
Affiliations
  • George Washington University (US)
  • George Washington University Hospital (US)
ORCID
Venue
Breast Cancer Research and Treatment
Publisher
Springer Science and Business Media LLC
Published
2000-01
Volume
59
Issue
1
Pages
15-26
ISSN
  • 0167-6806 (ISSN-L)
  • 1573-7217
DOI
10.1023/a:1006332011207
OpenAlex
W1997500225
Cited by
338
References
65
Citations by year
2026: 4 · 2025: 6 · 2024: 8 · 2023: 8 · 2022: 9 · 2021: 10 · 2020: 20 · 2019: 15 · 2018: 13 · 2017: 14 · 2016: 13 · 2015: 21 · 2014: 26 · 2013: 19 · 2012: 26
FWCI
1.16
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Breast Cancer Research and Treatment (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
GRP78, breast cancer, benign breast disease, estrogen receptor status, tumor microenvironment, apoptosis resistance, chemoresistance, topoisomerase II inhibitors, tumor aggressiveness
MeSH terms
Endoplasmic Reticulum Chaperone BiP, Adult, Aged, Breast Diseases, Breast Neoplasms, Carrier Proteins, Female, Heat-Shock Proteins, Humans, Immunohistochemistry, Middle Aged, Neoplasm Proteins, Gene Expression Regulation, Neoplastic, Apoptosis, Molecular Chaperones, HSP70 Heat-Shock Proteins

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.