ArticleCellular and molecular life sciences : CMLS2021
DHX9 contributes to the malignant phenotypes of colorectal cancer via activating NF-κB signaling pathway.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 90 citations in OpenAlex.
- Super-enhancer landscape regulated by CDK12 drives retinoblastoma progression.British journal of cancer · 2026Article
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- R-loops in colorectal cancer: mechanisms, mapping strategies, and therapeutic opportunities.Molecular biology reports · 2026Review
- A dsRNA Viral Transcriptional Regulator Evades Innate Immunity by Hijacking Host CoTranscription Factor DHX9.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ubc9-Mediated SUMOylation of RPL3, an Unappreciated Mechanism against Hepatocyte Senescence by Repressing the DHX9-p16 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Advantages, applications, and future directions ofMolecular therapy. Nucleic acids · 2025Review
- RP11-439C15.4 inhibits the malignant progression of hepatocellular carcinoma via binding to DHX9 and facilitating its degradation.Acta biochimica et biophysica Sinica · 2025Article
- DHX9-mediated epigenetic silencing of BECN1 contributes to impaired autophagy and tumor progression in breast cancer via recruitment of HDAC5.Cell death & disease · 2025Article
- Effects of solamargine in hepatic metastasis of colorectal cancer: induction of ferroptosis and elimination of cancer stem cells.Chinese medicine · 2025Article
- Discovery of ATX968: An Orally Available Allosteric Inhibitor of DHX9.Journal of medicinal chemistry · 2025Article
- Competitive binding between DDX21 and SIRT7 enhances NAT10-mediated acCell death & disease · 2025Article
- Integrative Transcriptome-Wide Association Study With Expression Quantitative Trait Loci Colocalization Identifies a Causal VAMP8 Variant for Nasopharyngeal Carcinoma Susceptibility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A Potent, Selective, Small-Molecule Inhibitor of DHX9 Abrogates Proliferation of Microsatellite Instable Cancers with Deficient Mismatch Repair.Cancer research · 2025Article
- Targeting Hepatocellular Carcinoma Growth: Haprolid's Inhibition of AKT Signaling Through DExH-Box Helicase 9 Downregulation.Cancers · 2025Article
- [High expression of AURKB promotes malignant phenotype of osteosarcoma cells by activating nuclear factor-κB signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Multi-omics reveals lactylation-driven regulatory mechanisms promoting tumor progression in oral squamous cell carcinoma.Genome biology · 2024Article
- Positive feedback loop of c-myc/XTP6/NDH2/NF-κB to promote malignant progression in glioblastoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Effects of super-enhancers in cancer metastasis: mechanisms and therapeutic targets.Molecular cancer · 2024Review
- cAMP-phosphodiesterase 4D7 (PDE4D7) forms a cAMP signalosome complex with DHX9 and is implicated in prostate cancer progression.Molecular oncology · 2024Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is the leading cause of cancer-related mortality worldwide, which makes it urgent to identify novel therapeutic targets for CRC treatment. In this study, DHX9 was filtered out as the prominent proliferation promoters of CRC by siRNA screening. Moreover, DHX9 was overexpressed in CRC cell lines, clinical CRC tissues and colitis-associated colorectal cancer (CAC) mouse model. The upregulation of DHX9 was positively correlated with poor prognosis in patients with CRC. Through gain- and loss-of function experiments, we found that DHX9 promoted CRC cell proliferation, colony formation, apoptosis resistance, migration and invasion in vitro. Furthermore, a xenograft mouse model and a hepatic metastasis mouse model were utilized to confirm that forced overexpression of DHX9 enhanced CRC outgrowth and metastasis in vivo, while DHX9 ablation produced the opposite effect. Mechanistically, from one aspect, DHX9 enhances p65 phosphorylation, promotes p65 nuclear translocation to facilitate NF-κB-mediated transcriptional activity. From another aspect, DHX9 interacts with p65 and RNA polymerase II (RNA Pol II) to enhance the downstream targets of NF-κB (e.g., Survivin, Snail) expression to potentiate the malignant phenotypes of CRC. Together, our results suggest that DHX9 may be a potential therapeutic target for prevention and treatment of CRC patients.
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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.