ArticleInternational journal of molecular sciences2017
Blockage of Glyoxalase I Inhibits Colorectal Tumorigenesis and Tumor Growth via Upregulation of STAT1, p53, and Bax and Downregulation of c-Myc and Bcl-2.
Article in International journal of molecular sciences, 2017. 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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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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Biological activity, UHPLC-MS phytochemical profiling, and computational studies of the leaf extract of Acridocarpus socotranus.Scientific reports · 2025Article
- Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025Review
- Article
- Development of pathway-oriented screening to identify compounds to control 2-methylglyoxal metabolism in tumor cells.Communications chemistry · 2023Article
- Identification of HAGHL as a novel metabolic oncogene regulating human colorectal cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Glyoxalase 1 as a Therapeutic Target in Cancer and Cancer Stem Cells.Molecules and cells · 2022Review
- Glyoxalase 1 knockdown induces age-related β-cell dysfunction and glucose intolerance in mice.EMBO reports · 2022Article
- Methylglyoxal Levels in Human Colorectal Precancer and Cancer: Analysis of Tumor and Peritumor Tissue.Life (Basel, Switzerland) · 2021Article
- The Dual-Role of Methylglyoxal in Tumor Progression - Novel Therapeutic Approaches.Frontiers in oncology · 2021Review
- Fra-1 Inhibits Cell Growth and the Warburg Effect in Cervical Cancer Cells via STAT1 Regulation of the p53 Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
- Transmembrane and Ubiquitin-Like Domain Containing 1 Protein (TMUB1) Negatively Regulates Hepatocellular Carcinoma Proliferation via Regulating Signal Transducer and Activator of Transcription 1 (STAT1).Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Reactive metabolite production is a targetable liability of glycolytic metabolism in lung cancer.Nature communications · 2019Article
- TPX2 silencing exerts anti‑tumor effects on hepatocellular carcinoma by regulating the PI3K/AKT signaling pathway.International journal of molecular medicine · 2019Article
- Liraglutide Treatment Ameliorates Neurotoxicity Induced by Stable Silencing of Pin1.International journal of molecular sciences · 2019Article
- Long Noncoding RNAs in Colorectal Adenocarcinoma; an in silico Analysis.Pathology oncology research : POR · 2019Article
- Role of MYC-miR-29-B7-H3 in Medulloblastoma Growth and Angiogenesis.Journal of clinical medicine · 2019Article
- Cancer/testis Antigen MAGEA3 Interacts with STAT1 and Remodels the Tumor Microenvironment.International journal of medical sciences · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GlyoxalaseI (GLOI) is an enzyme that catalyzes methylglyoxal metabolism. Overexpression of GLOI has been documented in numerous tumor tissues, including colorectal cancer (CRC). The antitumor effects of GLOI depletion have been demonstrated in some types of cancer, but its role in CRC and the mechanisms underlying this activity remain largely unknown. Our purpose was to investigate the antitumor effects of depleted GLOI on CRC in vitro and in vivo. RNA interference was used to deplete GLOI activity in four CRC cell lines. The cells' proliferation, apoptosis, migration, and invasion were assessed by using the Cell Counting Kit-8, plate colony formation assay, flow cytometry, and transwell assays. Protein and mRNA levels were analyzed by western blot and quantitative real-time PCR (qRT-PCR), respectively. The antitumor effect of GLOI depletion in vivo was investigated in a SW620 xenograft tumor model in BALB/c nude mice. Our results show that GLOI is over-expressed in the CRC cell lines. GLOI depletion inhibited the proliferation, colony formation, migration, and invasion and induced apoptosis of all CRC cells compared with the controls. The levels of signal transducer and activator of transcription 1 (STAT1), p53, and Bcl-2 assaciated X protein (Bax) were upregulated by GLOI depletion, while cellular homologue of avian myelocytomatosis virus oncogene (c-Myc) and B cell lymphoma/lewkmia-2 (Bcl-2) were downregulated. Moreover, the growth of SW620-induced CRC tumors in BALB/c nude mice was significantly attenuated by GLOI depletion. The expression levels of STAT1, p53, and Bax were increased and those of c-Myc and Bcl-2 were decreased in the GLOI-depleted tumors. Our findings demonstrate that GLOI depletion has an antitumor effect through the STAT1 or p53 signaling pathways in CRC, suggesting that GLOI is a potential therapeutic target.
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