ArticleMolecular cancer therapeutics2008
Nordihydroguaiaretic acid, a cytotoxic insulin-like growth factor-I receptor/HER2 inhibitor in trastuzumab-resistant breast cancer.
Article in Molecular cancer therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Impact of Nordihydroguaiaretic Acid on Proliferation, Energy Metabolism, and Chemosensitization in Non-Small-Cell Lung Cancer (NSCLC) Cell Lines.International journal of molecular sciences · 2024Article
- Role of Molecular Targeted Therapeutic Drugs in Treatment of Breast Cancer: A Review Article.Global medical genetics · 2023Review
- Nordihydroguaiaretic acid inhibits glyoxalase I, and causes the accumulation of methylglyoxal followed by cell-growth inhibition.Molecular biology reports · 2022Article
- The PolyphenolsMolecules (Basel, Switzerland) · 2021Article
- Nordihydroguaiaretic Acid: From Herbal Medicine to Clinical Development for Cancer and Chronic Diseases.Frontiers in pharmacology · 2020Review
- Acquired resistance mechanisms to afatinib in HER2-amplified gastric cancer cells.Cancer science · 2019Article
- Nordihydroguaiaretic acid impairs prostate cancer cell migration and tumor metastasis by suppressing neuropilin 1.Oncotarget · 2016Article
- Lapatinib sensitivities of two novel trastuzumab-resistant HER2 gene-amplified gastric cancer cell lines.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2014Article
- P38 MAPK contributes to resistance and invasiveness of HER2- overexpressing breast cancer.Current medicinal chemistry · 2014Article
- Anti-cancer IAP antagonists promote bone metastasis: a cautionary tale.Journal of bone and mineral metabolism · 2013Review
- Mechanisms of Adipocytokine-Mediated Trastuzumab Resistance in HER2-Positive Breast Cancer Cell Lines.Current pharmacogenomics and personalized medicine · 2013Article
- Targeting insulin and insulin-like growth factor signaling in breast cancer.Journal of mammary gland biology and neoplasia · 2012Review
- Selective inhibition of HER2-positive breast cancer cells by the HIV protease inhibitor nelfinavir.Journal of the National Cancer Institute · 2012Article
- New developments in the treatment of HER2-positive breast cancer.Breast cancer (Dove Medical Press) · 2012Article
- Pharmacological strategies to overcome HER2 cross-talk and Trastuzumab resistance.Current medicinal chemistry · 2012Review
- Atypical teratoid rhabdoid tumor: current therapy and future directions.Frontiers in oncology · 2012Article
- Molecular Mechanisms of Trastuzumab-Based Treatment in HER2-Overexpressing Breast Cancer.ISRN oncology · 2012Article
- Deciphering the role of insulin-like growth factor-I receptor in trastuzumab resistance.Chemotherapy research and practice · 2012Article
- Growth differentiation factor 15 (GDF15)-mediated HER2 phosphorylation reduces trastuzumab sensitivity of HER2-overexpressing breast cancer cells.Biochemical pharmacology · 2011Article
- Targeting Bcl-2 in Herceptin-Resistant Breast Cancer Cell Lines.Current pharmacogenomics and personalized medicine · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The majority of patients with HER2-overexpressing metastatic breast cancer who initially respond to the HER2-targeted antibody trastuzumab show disease progression within 1 year. The identification of novel agents that effectively inhibit survival of cancer cells that have progressed on trastuzumab is critical for improving outcome for this patient population. In the current study, we show that the phenolic compound nordihydroguaiaretic acid (NDGA) promoted cell death of trastuzumab-naive and trastuzumab-refractory HER2-overexpressing breast cancer cells. NDGA induced DNA fragmentation, cleavage of poly(ADP-ribose) polymerase and caspase-3, and inhibition of colony formation. In addition, NDGA inhibited insulin-like growth factor-I and HER2 signaling in trastuzumab-refractory cells, with reduced downstream phosphatidylinositol-3 kinase/Akt signaling. Importantly, combination treatment with NDGA and trastuzumab suppressed proliferation and survival of trastuzumab-refractory cells to a greater degree than either agent alone, suggesting that NDGA increases the sensitivity of refractory cells to trastuzumab. Derivatives of NDGA are currently in clinical trial for other solid tumors. Our data strongly support further study of NDGA as a potential therapeutic against breast cancers that have progressed on trastuzumab.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.