ArticleCell death & disease2024
CBX4 plays a bidirectional role in transcriptional regulation and lung adenocarcinoma progression.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed.
- In vivo inhibition of TDO2 in fibroids results in widespread alteration in the tumor transcriptome.Clinical science (London, England : 1979) · 2026Article
- Article
- CBX4 facilitates EV71 replication by SUMOylation and stabilizing 3D polymerase.Frontiers in microbiology · 2026Article
- Transcriptomic Signatures in TP53 Positive and Negative Tumor Samples in NSCLC.Current gene therapy · 2025Article
- Protein post-translational modifications in serine synthetic pathway: functions and molecular mechanisms.Cell communication and signaling : CCS · 2025Review
- Unravelling the impact of the chromobox proteins in human cancers.Cell death & disease · 2025Review
- Accelerated epigenetic aging in Huntington's disease involves polycomb repressive complex 1.Nature communications · 2025Article
- L-serine metabolic regulation and host respiratory homeostasis.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Understanding the dysregulated epigenetics governing LUAD progression is pivotal for identifying therapeutic targets. CBX4, a chromobox protein, is reported to be upregulated in LUAD. This study highlights the dual impact of CBX4 on LUAD proliferation and metastasis through a series of rigorous in vitro and in vivo experiments. Further investigation into the underlying mechanism through high-throughput ChIP-seq and RNA-seq reveals that CBX4 functions in promoting LUAD proliferation via upregulating PHGDH expression and subsequent serine biosynthesis, while concurrently suppressing LUAD metastasis by inhibiting ZEB2 transcription. CBX4 facilitates PHGDH transcription through the interaction with GCN5, inducing heightened histone acetylation on the PHGDH promoter. Simultaneously, the inhibition of ZEB2 transcription involves CBX4-mediated recruitment of canonical PRC1 (cPRC1), establishing H2K119ub on the ZEB2 promoter. These findings underscore CBX4's pivotal role as a regulator of LUAD progression, emphasizing its diverse transcriptional regulatory functions contingent upon interactions with specific epigenetic partners. Understanding the nuanced interplay between CBX4 and epigenetic factors sheds light on potential therapeutic avenues in LUAD.
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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.