ReviewJournal of experimental & clinical cancer research : CR2025
CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.
Review in Journal of experimental & clinical cancer research : CR, 2025. 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.
- LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.American journal of translational research · 2026Article
- Chromatin remodeling in bone organoids: from epigenetic regulation to disease modeling and therapeutic translation.Frontiers in genetics · 2026Review
- Targeting CHD1L suppresses prostate cancer progression via the FOXO3-PUMA axis.Journal of translational medicine · 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
5 authors.
Funding
Abstract
Chromodomain Helicase DNA-binding protein 1-Like (CHD1L) is a chromatin remodeling enzyme increasingly recognized as an oncogenic factor promoting tumor progression and metastatic potential by orchestrating transcriptional programs that drive epithelial-mesenchymal transition (EMT), cytoskeletal remodeling, and metastatic dissemination. In parallel, CHD1L has emerged as a master regulator of tumor cell survival by regulating DNA damage response and repair and enforcing G1 cell cycle progression. Furthermore, CHD1L plays a key role in immune evasion pathways by regulating signaling cascades and by suppressing both apoptotic and non-apoptotic cell death. In particular, CHD1L is a key suppressor of PARthanatos, a caspase-independent mechanism triggered by poly(ADP-ribose) (PAR) polymer fragmentation and apoptosis-inducing factor (AIF) activation. By regulating SPOCK1, MDM2, and TCTP, CHD1L further supports survival under cellular stress. Its overexpression correlates with metastasis, therapy resistance, and poor prognosis across many solid tumors. This review covers CHD1L's structure, oncogenic functions, and developmental origins, and highlights emerging therapeutic strategies that target CHD1L as a druggable vulnerability in cancer.
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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.