ArticleCancers2022
Restoring FAS Expression via Lipid-Encapsulated FAS DNA Nanoparticle Delivery Is Sufficient to Suppress Colon Tumor Growth In Vivo.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Co-stimulatory signal deficiency impairs cytotoxic T lymphocyte function in tumor immune evasion: molecular mechanisms and therapeutic implications.Journal of translational medicine · 2026Review
- Recent Developments in Lipid Nanoparticle-Mediated Delivery of Biotherapeutics and Gene Therapy Across the Blood-Brain Barrier.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- The Fas-FasL system: from apoptosis regulator to therapeutic target in autoimmunity, cancer, and transplantation.Immunologic research · 2026Review
- Lipid Nanoparticle Fas Gene Therapy Suppresses Autoimmune Lymphoproliferative Syndrome in Mice.Blood immunology & cellular therapy · 2025Article
- Lipid nanoparticle-delivered IFNα2 activates Cxcl9 to increase T cell tumor recruitment to suppress lung metastasis.Journal for immunotherapy of cancer · 2025Article
- The PRC2 complex epigenetically silences GATA4 to suppress cellular senescence and promote the progression of breast cancer.Translational oncology · 2024Article
- Research Advances of Lipid Nanoparticles in the Treatment of Colorectal Cancer.International journal of nanomedicine · 2024Review
- Diet effects on colonic health influence the efficacy of Bin1 mAb immunotherapy for ulcerative colitis.Scientific reports · 2023Article
- Improving cell and gene therapy safety and performance using next-generation Nanoplasmid vectors.Molecular therapy. Nucleic acids · 2023Review
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- Lipid Nanoparticle Delivery of Fas Plasmid Restores Fas Expression to Suppress Melanoma GrowthACS nano · 2022Article
- Amino acid metabolism genes associated with immunotherapy responses and clinical prognosis of colorectal cancer.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark of human colorectal cancer is lost expression of FAS, the death receptor for FASL of cytotoxic T lymphocytes (CTLs). However, it is unknown whether restoring FAS expression alone is sufficient to suppress csolorectal-cancer development. The FAS promoter is hypermethylated and inversely correlated with FAS mRNA level in human colorectal carcinomas. Analysis of single-cell RNA-Seq datasets revealed that FAS is highly expressed in epithelial cells and immune cells but down-regulated in colon-tumor cells in human colorectal-cancer patients. Codon usage-optimized mouse and human FAS cDNA was designed, synthesized, and encapsulated into cationic lipid to formulate nanoparticle DOTAP-Chol-mFAS and DOTAP-Chol-hFAS, respectively. Overexpression of codon usage-optimized FAS in metastatic mouse colon-tumor cells enabled FASL-induced elimination of FAS
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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.