Evidence map›Paper›PMID 37596619›Full record

ReviewJournal of experimental & clinical cancer research : CR2023

Role of the DEAD-box RNA helicase DDX5 (p68) in cancer DNA repair, immune suppression, cancer metabolic control, virus infection promotion, and human microbiome (microbiota) negative influence.

Fengzhi Li, Xiang Ling, Sayan Chakraborty, Christos Fountzilas, Jianmin Wang, Anmbreen Jamroze, Xiaozhuo Liu, Pawel Kalinski, Dean G Tang

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 39 citations in OpenAlex.

  1. Unveiling the Immune Mechanisms of Hypertension With Single-Cell Transcriptome-Wide Mendelian Randomization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Multi-omics analysis of HLTF context-dependent regulation across TCGA cohorts revealed its potential as new biomarker in tumour.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
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  9. Human lncRNAProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Advantages, applications, and future directions ofMolecular therapy. Nucleic acids · 2025
    Review
  15. Article
  16. Article
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  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Fengzhi LiDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA. fengzhi.li@roswellpark.org.ORCID http://orcid.org/0000-0002-2299-7951
Xiang LingDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Sayan ChakrabortyDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Christos FountzilasProgram of Developmental Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA.
Jianmin WangDepartment of Bioinformatics & Biostatistics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA.
Anmbreen JamrozeDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Xiaozhuo LiuDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Pawel KalinskiDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA.
Dean G TangDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI CANDACE S JOHNSON · 1985 to 2026
$116.6M
Novel Therapeutic Strategies to Co-Target Undifferentiated Prostate Cancer (PCa) Stem Cells and Bulk PCa CellsR01CA240290 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 2019 to 2026
$3.1M
A small molecule broad spectrum inhibitor of antiapoptotic genes to treat cancerR44CA176937 · NCI · CANGET BIOTEKPHARMA, LLC · PI LI, FENGZHI, LING, XIANG · 2014 to 2018
$2.3M
Tumor-Suppressive Functions and Molecular Regulation of LRIG1 in Prostate Cancer and CRPCR01CA237027 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI TANG, DEAN G. · 2019 to 2023
$2.2M
Perform non-GLP and GLP TOX/TK studies, and file a novel drug IND with the FDA for advanced pancreatic cancer patient clinical trialsR43CA275410 · NCI · CANGET BIOTEKPHARMA, LLC · PI LI, FENGZHI, LING, XIANG · 2023 to 2023
$400k
NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA237027NCI NIH HHS R01 CA240290NCI NIH HHS R43 CA275410NCI NIH HHS R44 CA176937Pancreatic Cancer Action Network 20-65-FENG
6 · The paper itself

Abstract

There is increasing evidence indicating the significant role of DDX5 (also called p68), acting as a master regulator and a potential biomarker and target, in tumorigenesis, proliferation, metastasis and treatment resistance for cancer therapy. However, DDX5 has also been reported to act as an oncosuppressor. These seemingly contradictory observations can be reconciled by DDX5's role in DNA repair. This is because cancer cell apoptosis and malignant transformation can represent the two possible outcomes of a single process regulated by DDX5, reflecting different intensity of DNA damage. Thus, targeting DDX5 could potentially shift cancer cells from a growth-arrested state (necessary for DNA repair) to apoptosis and cell killing. In addition to the increasingly recognized role of DDX5 in global genome stability surveillance and DNA damage repair, DDX5 has been implicated in multiple oncogenic signaling pathways. DDX5 appears to utilize distinct signaling cascades via interactions with unique proteins in different types of tissues/cells to elicit opposing roles (e.g., smooth muscle cells versus cancer cells). Such unique features make DDX5 an intriguing therapeutic target for the treatment of human cancers, with limited low toxicity to normal tissues. In this review, we discuss the multifaceted functions of DDX5 in DNA repair in cancer, immune suppression, oncogenic metabolic rewiring, virus infection promotion, and negative impact on the human microbiome (microbiota). We also provide new data showing that FL118, a molecular glue DDX5 degrader, selectively works against current treatment-resistant prostate cancer organoids/cells. Altogether, current studies demonstrate that DDX5 may represent a unique oncotarget for effectively conquering cancer with minimal toxicity to normal tissues.

Indexed as

DEAD-box RNA HelicasesMicrobiotaCell Transformation, NeoplasticDNA RepairHumansImmunosuppression TherapyMaleProstatic NeoplasmsSignal TransductionDdx5 protein, humanDEAD-box RNA HelicasesCancer metabolic controlCancer therapeuticsDDX5DDX5 degrader FL118DNA repairImmune suppressionMicrobiota negative influenceOncotargetp68Virus infection promotion

Identifiers

PMID37596619
PMCPMC10439624
OpenAlexW4385997304

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.