ArticleGlycobiology2019
Transcriptional activation of fucosyltransferase (FUT) genes using the CRISPR-dCas9-VPR technology reveals potent N-glycome alterations in colorectal cancer cells.
Article in Glycobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 42 citations in OpenAlex.
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- CRISPR-driven diagnostics: Molecular mechanisms, clinical efficacy and translational challenges.Clinical and translational medicine · 2025Review
- CRISPR/Cas9 in colorectal cancer: Revolutionizing precision oncology through genome editing and targeted therapeutics.Iranian journal of basic medical sciences · 2025Review
- High-Throughput Mass Spectrometry Analysis ofJournal of proteome research · 2024Article
- CRISPR-Cas9 in basic and translational aspects of cancer therapy.BioImpacts : BI · 2024Review
- Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway.Heliyon · 2023Article
- Evaluation of a Novel Oncolytic Adenovirus SilencingInternational journal of molecular sciences · 2022Article
- Current updates of CRISPR/Cas9-mediated genome editing and targeting within tumor cells: an innovative strategy of cancer management.Cancer communications (London, England) · 2022Review
- Integration of CRISPR/Cas9 with artificial intelligence for improved cancer therapeutics.Journal of translational medicine · 2022Review
- Intestinal Norovirus Binding Patterns in Nonsecretor Individuals.Journal of virology · 2022Article
- Hyperglycemia alters N-glycans on colon cancer cells through increased production of activated monosaccharides.Glycoconjugate journal · 2022Article
- Emerging glyco-based strategies to steer immune responses.The FEBS journal · 2021Review
- MiR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway.BMC cancer · 2021Article
- Up-Regulating ERIC by CRISPR-dCas9-VPR Inhibits Cell Proliferation and Invasion and Promotes Apoptosis in Human Bladder Cancer.Frontiers in molecular biosciences · 2021Article
- CRISPR/Cas9: A powerful genome editing technique for the treatment of cancer cells with present challenges and future directions.Life sciences · 2020Review
- Article
- CRISPR/Cas system: An emerging technology in stem cell research.World journal of stem cells · 2019Review
- Review
- MiR-29b/Sp1/FUT4 axis modulates the malignancy of leukemia stem cells by regulating fucosylation via Wnt/β-catenin pathway in acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2019Article
- Genetic glycoengineering in mammalian cells.The Journal of biological chemistryReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant fucosylation in cancer cells is considered as a signature of malignant cell transformation and it is associated with tumor progression, metastasis and resistance to chemotherapy. Specifically, in colorectal cancer cells, increased levels of the fucosylated Lewisx antigen are attributed to the deregulated expression of pertinent fucosyltransferases, like fucosyltransferase 4 (FUT4) and fucosyltransferase 9 (FUT9). However, the lack of experimental models closely mimicking cancer-specific regulation of fucosyltransferase gene expression has, so far, limited our knowledge regarding the substrate specificity of these enzymes and the impact of Lewisx synthesis on the glycome of colorectal cancer cells. Therefore, we sought to transcriptionally activate the Fut4 and Fut9 genes in the well-known murine colorectal cancer cell line, MC38, which lacks expression of the FUT4 and FUT9 enzymes. For this purpose, we utilized a physiologically relevant, guide RNA-based model of de novo gene expression, namely the CRISPR-dCas9-VPR system. Induction of the Fut4 and Fut9 genes in MC38 cells using CRISPR-dCas9-VPR resulted in specific neo-expression of functional Lewisx antigen on the cell surface. Interestingly, Lewisx was mainly carried by N-linked glycans in both MC38-FUT4 and MC38-FUT9 cells, despite pronounced differences in the biosynthetic properties and the expression stability of the induced enzymes. Moreover, Lewisx expression was found to influence core-fucosylation, sialylation, antennarity and the subtypes of N-glycans in the MC38-glycovariants. In conclusion, exploiting the CRISPR-dCas9-VPR system to augment glycosyltransferase expression is a promising method of transcriptional gene activation with broad application possibilities in glycobiology and oncology research.
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.