ArticleBiomolecules2025
HDGF Knockout Suppresses Colorectal Cancer Progression and Drug Resistance by Modulating the DNA Damage Response.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- Lactylation-driven metabolic reprogramming promotes osteosarcoma malignancy via HDGF-mediated proliferation and immune modulation.Frontiers in immunology · 2026Article
- Dynamics and regulatory role of 5-methylcytosine modification in mRNA colocalized with RNA G-quadruplex structure in mouse development.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Oncogenic Role and Drug Resistance Effect of CCDC6 in iCCA: Potential Strategies for Targeted Intervention.Journal of cellular and molecular medicine · 2025Article
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
- Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.Frontiers in cell and developmental biology · 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
7 authors.
Funding
Abstract
Colorectal cancer (CRC) is a highly heterogeneous gastrointestinal malignancy. Despite significant advances in molecular targeted therapies for CRC in recent years, the increase in the overall survival rates for CRC patients remains limited. Therefore, there is an urgent need to explore novel drug targets. Herein, we show that heparin binding growth factor (HDGF) is highly expressed in CRC, and that its overexpression is associated with a poor disease-free interval. Additionally, we reveal that HDGF knockout reduces proliferation, migration, and invasion, while enhancing apoptosis in CRC cells, thereby validating HDGF as a potential therapeutic target for CRC. Mechanistically, we found that HDGF modulates DNA damage response and, by recruiting C-terminal binding protein-interacting protein (CtIP), it facilitates homologous recombination repair to influence CRC drug sensitivity. Furthermore, we propose that HDGF may serve as a recognition protein for H3K36me3, participating in the repair of damaged transcriptionally active genes, thus maintaining genomic stability in CRC.
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.