ArticleInternational journal of biological sciences2025
Oncogenic RARγ isoforms promote head and neck cancer proliferation through vinexin-β-mediated cell cycle acceleration and autocrine activation of EGFR signal.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Retinoic Acid Receptor γ Is a Ligand-Activated Gatekeeper to Stem Cell Developmental Progression.International journal of molecular sciences · 2026Review
- TMEM33 regulates the proliferation and migration of lung adenocarcinoma by promoting the PI3K/AKT/mTOR signaling pathway.Cancer cell international · 2026Article
- The Influences of RARγ on the Behavior of Normal and Cancer Stem Cells.International journal of molecular sciences · 2026Review
- The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Results of retinoid-based therapies in head and neck cancer (HNC) are generally disappointing, indicating a lack of understanding of retinoic acid signaling. The role of retinoic acid receptor gamma (RARγ) and its isoforms in HNC is yet to be established. In this study, we found that RARγ1, 2, 4 are the predominant RARγ isoforms expressed in various types of human cancers, including HNC. The mechanistic study revealed that RARγ1, 2, 4 enhanced the proliferation of HNC cells by accelerating cell cycle progression through interaction with vinexin-β, as well as by ligand-dependent activation of EGFR with downstream Akt, ERK, Src, and YAP signaling pathways. Retinoic acid binding and CDK7-dependent phosphorylation on specific serine residue at the AF-1 domain are mandatory for RARγ-mediated growth promotion of HNC. Knockdown of RARγ abolished proliferation of cultured HNC cells, and completely prevented tumor growth in xenografted nude mice. Similar effects were observed in various human cancer types other than HNC. Our results indicate that RARγ-targeting approach could be a promising therapeutic and chemopreventive strategy for human cancers.
Indexed as
Identifiers
What Socratic holds
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.