ArticleCell death and differentiation2020
Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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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
9 citing papers in PubMed.
- Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025Article
- Evaluation of the safety and efficacy ofFrontiers in immunology · 2025Article
- Integration of Bulk and Single-Cell Transcriptomics Reveals BCL2L14 as a Novel IGKC+ T Cell-Associated Therapeutic Target in Breast Cancer.Journal of inflammation research · 2025Article
- Identification of Serum Biomarkers to Monitor Therapeutic Response in Intestinal-Type Gastric Cancer.International journal of molecular sciences · 2024Article
- BCL-G: 20 years of research on a non-typical protein from the BCL-2 family.Cell death and differentiation · 2023Review
- Confocal Endomicroscopy Monitoring of Tumor Formation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Necroptosis is dispensable for the development of inflammation-associated or sporadic colon cancer in mice.Cell death and differentiation · 2021Article
- Inhibition of histone methyltransferase G9a attenuates liver cancer initiation by sensitizing DNA-damaged hepatocytes to p53-induced apoptosis.Cell death & disease · 2021Article
- BCL-2 family deregulation in colorectal cancer: potential for BH3 mimetics in therapy.Apoptosis : an international journal on programmed cell death · 2020Review
Corrections and comments
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Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal epithelial cells provide a selective barrier that segregates the host immune system from luminal microorganisms, thereby contributing directly to the regulation of homeostasis. We have shown that from early embryonic development Bcl-G, a Bcl-2 protein family member with unknown function, was highly expressed in gastrointestinal epithelial cells. While Bcl-G was dispensable for normal growth and development in mice, the loss of Bcl-G resulted in accelerated progression of colitis-associated cancer. A label-free quantitative proteomics approach revealed that Bcl-G may contribute to the stability of a mucin network, which when disrupted, is linked to colon tumorigenesis. Consistent with this, we observed a significant reduction in Bcl-G expression in human colorectal tumors. Our study identifies an unappreciated role for Bcl-G in colon cancer.
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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.