ArticleMolecular endocrinology (Baltimore, Md.)2009
HIC1 regulates tumor cell responses to endocrine therapies.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- The important molecular markers on chromosome 17 and their clinical impact in breast cancer.International journal of molecular sciences · 2011Review
- Cytotoxic Activities of Silver Nanoparticles and Silver Ions in Parent and Tamoxifen-Resistant T47D Human Breast Cancer Cells and Their Combination Effects with Tamoxifen against Resistant Cells.Avicenna journal of medical biotechnology · 2010Article
Corrections and comments
- Retraction · 2011-08-11Falsification/Fabrication of Data · Falsification/Fabrication of Image · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author ·
- Commented on by
- Commented on by
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
An intractable problem impeding breast cancer treatment by the most frequently prescribed endocrine therapy tamoxifen is the inevitable development of resistance, and the molecular mechanisms underlying this loss of responsiveness by breast cancers have been under intense investigation but are not yet fully elucidated. Our recent reports demonstrated that the tumor suppressor heavily methylated in cancers 1 (HIC1) plays an essential role in growth suppression mediated by external stimuli. We report here that novel tumor suppressor HIC1 is required for growth suppression by estrogen antagonists in breast cancer cells. We also find that HIC1 expression is dramatically induced by exposure to estrogen antagonists in sensitive cells, via a c-Jun N-terminal kinase 1 (JNK1) and prohibitin-mediated signaling pathway. This induction is lost in spontaneously antagonist-resistant breast cancer cells. Furthermore, reintroducing HIC1 into resistant breast cancer cells restored their sensitivity to the estrogen antagonists, indicating the existence of a novel regulatory mechanism for growth control of breast cancer cells.
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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.