ArticleCancer cell2023
Transcriptional-translational conflict is a barrier to cellular transformation and cancer progression.
Article in Cancer cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Article
- SPEN inactivation drives resistance to androgen receptor pathway inhibitors in metastatic prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Rasgrp1-Mediated Dampening of EGFR Signals Supports Coordinated Mammary Gland Development.Cells · 2026Article
- ARID1A loss drives gastric signet ring cell carcinoma by regulating mucin production and secretion.Nature communications · 2026Article
- Club Cells in Nasal Epithelial Repair: Insights From an IL-13-Induced Inflammatory Model.Allergy · 2026Article
- Ferroptosis as a therapeutic vulnerability in ARID1A-deficient bladder cancer.Communications biology · 2026Article
- Deep learning-based non-invasive profiling of tumor transcriptomes from cell-free DNA for precision oncology.bioRxiv : the preprint server for biology · 2026Article
- Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R-Loop Accumulation and DNA Repair Deficiencies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SWI/SNF-associated molecular subtypes reshape tumor microenvironmental features and inform precision therapeutic strategies in bladder cancer.Frontiers in cellular and infection microbiology · 2026Article
- Integration of transcriptome profiling to identify key genes involved in the interplay between oxidative stress and mitophagy in major depressive disorder, followed by multidimensional phenotypic validation.Frontiers in psychiatry · 2026Article
- Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal-like and malignant urothelial cells.Molecular oncology · 2025Article
- Ten mouse organs proteome and metabolome atlas from adult to aging.Genome medicine · 2025Article
- Lysyl-tRNA synthetase orchestrates translation and hormone signaling during reproduction in Aedes aegypti mosquitoes.Communications biology · 2025Article
- Vitamin K2 Alleviates Insulin Resistance Associated Skeletal Muscle Atrophy via the AKT/mTOR Signalling Pathway.Journal of cachexia, sarcopenia and muscle · 2025Article
- HMGA2 and protein leucine methylation drive pancreatic cancer lineage plasticity.Nature communications · 2025Article
- SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- Ribosome-directed cancer therapies: the tip of the iceberg?Trends in pharmacological sciences · 2025Review
- Clinical and Prognostic Value of VHL in Korean Patients with Rectal Cancer.Medicina (Kaunas, Lithuania) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 5 institutions in 2 countries.
Funding
Abstract
We uncover a tumor-suppressive process in urothelium called transcriptional-translational conflict caused by deregulation of the central chromatin remodeling component ARID1A. Loss of Arid1a triggers an increase in a nexus of pro-proliferation transcripts, but a simultaneous inhibition of the eukaryotic elongation factor 2 (eEF2), which results in tumor suppression. Resolution of this conflict through enhancing translation elongation speed enables the efficient and precise synthesis of a network of poised mRNAs resulting in uncontrolled proliferation, clonogenic growth, and bladder cancer progression. We observe a similar phenomenon in patients with ARID1A-low tumors, which also exhibit increased translation elongation activity through eEF2. These findings have important clinical implications because ARID1A-deficient, but not ARID1A-proficient, tumors are sensitive to pharmacologic inhibition of protein synthesis. These discoveries reveal an oncogenic stress created by transcriptional-translational conflict and provide a unified gene expression model that unveils the importance of the crosstalk between transcription and translation in promoting cancer.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.