ArticlePloS one2016
Gasdermin C Is Upregulated by Inactivation of Transforming Growth Factor β Receptor Type II in the Presence of Mutated Apc, Promoting Colorectal Cancer Proliferation.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.
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Who cites it
138 citing papers in PubMed, 191 citations in OpenAlex.
- Igniting antitumour immunity with cancer cell pyroptosis.Nature reviews. Cancer · 2026Review
- Inflammatory and traditional risk factors associated with the progression of chronic kidney disease in patients with rheumatoid arthritis.Clinical and experimental nephrology · 2026Article
- Gasdermin-Mediated Pyroptosis: Novel Strategies Against Colorectal Cancer.Cancer science · 2026Review
- Theme and variations: activation and regulation of gasdermin-mediated inflammation.Biochemical Society transactions · 2026Review
- Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026Review
- LncRNA regulation of pyroptosis determines prognostic outcomes and functional characteristics in liver cancer.Discover oncology · 2026Article
- Identification of super-enhancer-based biomarkers for predicting survival and immunotherapy efficacy in colorectal cancer.Journal of Cancer · 2026Article
- Integrative PANoptosis-focused omics analysis uncovers GSDMC as a candidate biomarker in breast cancer.Frontiers in cell and developmental biology · 2026Article
- Review
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
- Single-dose DSS-induced inflammation enhances colorectal tumorigenesis in APC and KRAS mutant mice.Scientific reports · 2025Article
- From mechanism to application: programmed cell death pathways in nanomedicine-driven cancer therapies.Bioactive materials · 2025Review
- Development of Prognostic Features and Investigation of Therapeutic Insights Related to Non-Apoptotic Regulatory Cell Death in Colorectal Cancer.Applied biochemistry and biotechnology · 2025Article
- Mechanistic insights into gasdermin-mediated pyroptosis.Nature reviews. Molecular cell biology · 2025Review
- Targeting pyroptosis for cancer immunotherapy: mechanistic insights and clinical perspectives.Molecular cancer · 2025Review
- Caspase-6/Gasdermin C-Mediated Tumor Cell Pyroptosis Promotes Colorectal Cancer Progression Through CXCL2-Dependent Recruitment of Myeloid-Derived Suppressor Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Manipulation of cancer cell pyroptosis for therapeutic approaches: challenges and opportunities.Biomarker research · 2025Review
- Unveiling the nexus: pyroptosis and its crucial implications in liver diseases.Molecular and cellular biochemistry · 2025Review
- GSDMD-mediated pyroptosis: molecular mechanisms, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Molecular characteristics, clinical significance and cancer‑immune interactions of pyroptosis‑related genes in colorectal cancer.Oncology letters · 2025Article
78 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in TGFBR2, a component of the transforming growth factor (TGF)-β signaling pathway, occur in high-frequency microsatellite instability (MSI-H) colorectal cancer (CRC). In mouse models, Tgfbr2 inactivation in the intestinal epithelium accelerates the development of malignant intestinal tumors in combination with disruption of the Wnt-β-catenin pathway. However, no studies have further identified the genes influenced by TGFBR2 inactivation following disruption of the Wnt-β-catenin pathway. We previously described CDX2P-G19Cre;Apcflox/flox mice, which is stochastically null for Apc in the colon epithelium. In this study, we generated CDX2P-G19Cre;Apcflox/flox;Tgfbr2flox/flox mice, with simultaneous loss of Apc and Tgfbr2. These mice developed tumors, including adenocarcinoma in the proximal colon. We compared gene expression profiles between tumors of the two types of mice using microarray analysis. Our results showed that the expression of the murine homolog of GSDMC was significantly upregulated by 9.25-fold in tumors of CDX2P-G19Cre;Apcflox/flox;Tgfbr2flox/flox mice compared with those of CDX2P-G19Cre;Apcflox/flox mice. We then investigated the role of GSDMC in regulating CRC tumorigenesis. The silencing of GSDMC led to a significant reduction in the proliferation and tumorigenesis of CRC cell lines, whereas the overexpression of GSDMC enhanced cell proliferation. These results suggested that GSDMC functioned as an oncogene, promoting cell proliferation in colorectal carcinogenesis. In conclusion, combined inactivation of both Apc and Tgfbr2 in the colon epithelium of a CRC mouse model promoted development of adenocarcinoma in the proximal colon. Moreover, GSDMC was upregulated by TGFBR2 mutation in CRC and promoted tumor cell proliferation in CRC carcinogenesis, suggesting that GSDMC may be a promising therapeutic target.
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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.