ArticleMolecular cancer therapeutics2008
Cyclooxygenase inhibitors block uterine tumorigenesis in HMGA1a transgenic mice and human xenografts.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Flavopiridol induces BCL-2 expression and represses oncogenic transcription factors in leukemic blasts from adults with refractory acute myeloid leukemia.Leukemia & lymphoma · 2011Trial
- HMGA1 Activates FGFBP1 Transcription to Enhance Angiogenesis Induction and Tumor Progression via FGF2/FGFR1 Pathway.International journal of biological sciences · 2026Article
- HMGA1, Moonlighting Protein Function, and Cellular Real Estate: Location, Location, Location!Biomolecules · 2021Review
- HMGA Proteins in Hematological Malignancies.Cancers · 2020Review
- The effect of HMGA1 in LPS-induced Myocardial Inflammation.International journal of biological sciences · 2020Article
- High mobility group A1 (HMGA1) protein and gene expression correlate with ER-negativity and poor outcomes in breast cancer.Breast cancer research and treatment · 2020Article
- HMGA1 in cancer: Cancer classification by location.Journal of cellular and molecular medicine · 2019Review
- Lessons from the Crypt: HMGA1-Amping up Wnt for Stem Cells and Tumor Progression.Cancer research · 2018Review
- Mandatory role of HMGA1 in human airway epithelial normal differentiation and post-injury regeneration.Oncotarget · 2018Article
- The High Mobility Group A1 (HMGA1) gene is highly overexpressed in human uterine serous carcinomas and carcinosarcomas and drives Matrix Metalloproteinase-2 (MMP-2) in a subset of tumors.Gynecologic oncology · 2016Article
- The High Mobility Group A1 (HMGA1) Transcriptome in Cancer and Development.Current molecular medicine · 2016Review
- The high mobility group A1 molecular switch: turning on cancer - can we turn it off?Expert opinion on therapeutic targets · 2014Review
- Hitting the bull's eye: targeting HMGA1 in cancer stem cells.Expert review of anticancer therapy · 2014Article
- HMGA1: a master regulator of tumor progression in triple-negative breast cancer cells.PloS one · 2013Article
- HMGA1 reprograms somatic cells into pluripotent stem cells by inducing stem cell transcriptional networks.PloS one · 2012Article
- HMGA1 induces intestinal polyposis in transgenic mice and drives tumor progression and stem cell properties in colon cancer cells.PloS one · 2012Article
- HMGA1 drives stem cell, inflammatory pathway, and cell cycle progression genes during lymphoid tumorigenesis.BMC genomics · 2011Article
- AKNA: another AT-hook transcription factor "hooking-up" with inflammation.Cell research · 2011Article
- The high mobility group A1 gene: transforming inflammatory signals into cancer?Cancer research · 2010Review
- The high-mobility group A1a/signal transducer and activator of transcription-3 axis: an achilles heel for hematopoietic malignancies?Cancer research · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Uterine cancer is a common cause for cancer death in women and there is no effective therapy for metastatic disease. Thus, research is urgently needed to identify new therapeutic agents. We showed previously that all female HMGA1a transgenic mice develop malignant uterine tumors, indicating that HMGA1a causes uterine cancer in vivo. We also demonstrated that HMGA1a up-regulates cyclooxygenase-2 (COX-2) during tumorigenesis in this model. Similarly, we found that HMGA1a and COX-2 are overexpressed in human leiomyosarcomas, a highly malignant uterine cancer. Although epidemiologic studies indicate that individuals who take COX inhibitors have a lower incidence of some tumors, these inhibitors have not been evaluated in uterine cancer. Here, we show that HMGA1a mice on sulindac (a COX-1/COX-2 inhibitor) have significantly smaller uterine tumors than controls. To determine if COX inhibitors are active in human uterine cancers that overexpress HMGA1a, we treated cultured cells with sulindac sulfide or celecoxib (a specific COX-2 inhibitor). Both drugs block anchorage-independent growth in high-grade human uterine cancer cells that overexpress HMGA1a (MES-SA cells). In contrast, neither inhibitor blocked transformation in cells that do not overexpress HMGA1a. Moreover, xenograft tumors from MES-SA cells were significantly inhibited in mice on sulindac. More strikingly, no tumors formed in mice on celecoxib. These preclinical studies suggest that COX inhibitors could play a role in preventing tumor onset or progression in uterine cancers with dysregulation of the HMGA1a-COX-2 pathway. Importantly, these drugs have lower toxicity than chemotherapeutic agents used to treat advanced-stage uterine cancers.
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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 Socratic graph.