ArticleFrontiers in cell and developmental biology2022
Ferroptosis-Related Gene
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- MT1G promotes the progression of ccRCC by suppressing ferroptosis through activation of the PI3K-AKT pathway.Translational oncology · 2026Article
- Single-cell RNA sequencing reveals a B cell-related immunosuppressive landscape and a potential suppressor in hepatocellular carcinoma.Journal of translational medicine · 2025Article
- MT1G promotes iron autophagy and inhibits the function of gastric cancer cell lines by intervening in GPX4/SQSTM1.Scientific reports · 2024Article
- MT1G induces lipid droplet accumulation through modulation of H3K14 trimethylation accelerating clear cell renal cell carcinoma progression.British journal of cancer · 2024Article
- Exploring Predictive and Prognostic Biomarkers in Colorectal Cancer: A Comprehensive Review.Cancers · 2024Review
- Using a pan-cancer atlas to investigate tumour associated macrophages as regulators of immunotherapy response.Nature communications · 2024Article
- Article
- NFE2L2 and ferroptosis resistance in cancer therapy.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Research progress on ferroptosis in colorectal cancer.Frontiers in immunology · 2024Review
- Construction and Validation of Novel Ferroptosis-related Risk Score Signature and Prognostic Prediction Nomogram for Patients with Colorectal Cancer.International journal of medical sciences · 2024Article
- Ferroptosis: the balance between death and survival in colorectal cancer.International journal of biological sciences · 2024Review
- Metabolic reprogramming, autophagy, and ferroptosis: Novel arsenals to overcome immunotherapy resistance in gastrointestinal cancer.Cancer medicine · 2023Review
- Harnessing Ferroptosis to Overcome Drug Resistance in Colorectal Cancer: Promising Therapeutic Approaches.Cancers · 2023Review
- The Induction Mechanism of Ferroptosis, Necroptosis, and Pyroptosis in Inflammatory Bowel Disease, Colorectal Cancer, and Intestinal Injury.Biomolecules · 2023Review
- Ferroptosis-based nano delivery systems targeted therapy for colorectal cancer: Insights and future perspectives.Asian journal of pharmaceutical sciences · 2022Review
- Ferroptosis: Reviewing CRC with the Third Eye.Journal of inflammation research · 2022Review
- Screening of ferroptosis-related genes with prognostic effect in colorectal cancer by bioinformatic analysis.Frontiers in molecular biosciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis, a newly discovered way of cell death, has been proved to be involved in the oncogenesis and development of cancers, including colorectal cancer (CRC). Here, by identifying the differentially expressed genes (DEGs) from three CRC transcriptome microarray datasets (GSE20842, GSE23878, and GSE25070), we found that the expression of MT1G was significantly decreased in CRC tissues, and the patients with a high level of MT1G displayed a poor prognosis. Quantitative PCR (qPCR) further confirmed the downregulated MT1G in two CRC cells, HCT8 and HCT116. The colony-forming assay indicated that the MT1G overexpression exhibited a remarkable inhibition of cell proliferation in HCT8 and HCT116 cells. In addition, we explored the co-expressed genes of MT1G to gain a better understanding of its potential signaling pathways. Aberrantly expressed MT1G also affected the immune response of CRC patients. Collectively, these findings might deepen our comprehension on the potential biological implications of MT1G in CRC.
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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.