ArticleMolecular carcinogenesis2018
The Rb tumor suppressor regulates epithelial cell migration and polarity.
Article in Molecular carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Patterns in the tapestry of chromatin-bound RB.Trends in cell biology · 2024Review
- Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci and is redistributed by cell-cycle progression.Molecular cell · 2022Article
- Cell cycle expression of polarity genes features Rb targeting of Vang.Cells & development · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Altered cell polarity and migration are hallmarks of cancer and metastases. Here we show that inactivation of the retinoblastoma gene (Rb) tumor suppressor causes defects in tissue closure that reflect the inability of Rb null epithelial cells to efficiently migrate and polarize. These defects occur independently of pRB's anti-proliferative role and instead correlate with upregulation of RhoA signaling and mislocalization of apical-basal polarity proteins. Notably, concomitant inactivation of tp53 specifically overrides the motility defect, and not the aberrant polarity, thereby uncovering previously unappreciated mechanisms by which Rb and tp53 mutations cooperate to promote cancer development and metastases.
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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.