ArticleBreast cancer research : BCR2005
Antisense oligonucleotides targeting the progesterone receptor inhibit hormone-independent breast cancer growth in mice.
Article in Breast cancer research : BCR, 2005. 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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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.
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Who cites it
6 citing papers in PubMed, 29 citations in OpenAlex.
- Steroid profile in patients with breast cancer and in mice treated with mifepristone.Endocrine-related cancer · 2024Article
- Antiprogestins in gynecological diseases.Reproduction (Cambridge, England) · 2015Review
- Novel, low cost, highly effective, handmade steroid pellets for experimental studies.PloS one · 2013Article
- Involvement of α2- and β2-adrenoceptors on breast cancer cell proliferation and tumour growth regulation.British journal of pharmacology · 2012Article
- Inoculated mammary carcinoma-associated fibroblasts: contribution to hormone independent tumor growth.BMC cancer · 2010Article
- Progesterone receptor isoform functions in normal breast development and breast cancer.Critical reviews in eukaryotic gene expression · 2008Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPrevious data from our laboratory suggested that progesterone receptors (PRs) are involved in progestin-independent growth of mammary carcinomas. To investigate this possibility further, we studied the effects of PR antisense oligodeoxynucleotides (asPR) on in vivo tumor growth.
methodBALB/c mice with subcutaneous 25 mm2 mammary carcinomas expressing estrogen receptor-alpha and PR were either injected intraperitoneally with 1 mg asPR every 24 or 12 hours for 5-10 days, or subcutaneously with RU 486 (6.5 mg/kg body weight) every 24 hours. Control mice received vehicle or scPR.
resultsSignificant inhibition of tumor growth as well as a significant decrease in bromodeoxyuridine uptake was observed in asPR-treated mice, which correlated with histological signs of regression and increased apoptosis. Mice treated with RU 486 experienced almost complete tumor regression. No differences were detected between vehicle-treated and scPR-treated mice. Anti-progestin-treated and asPR-treated mice were in a continuous estrous/meta-estrous state. Decreased phosphorylated extracellular signal-regulated kinase (ERK)1 and ERK2 levels and estrogen receptor-alpha expression were observed as late events in RU 486-treated and asPR-treated mice with regressing tumors.
conclusionWe demonstrate, for the first time, inhibition of tumor growth in vivo using asPR. Our results provide further evidence for a critical and hierarchical role of the PR pathway in mammary carcinomas.
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