ArticleJournal of experimental & clinical cancer research : CR2020
Downregulation of GLYR1 contributes to microsatellite instability colorectal cancer by targeting p21 via the p38MAPK and PI3K/AKT pathways.
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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12 citing papers in PubMed, 20 citations in OpenAlex.
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- GLYR1-mediated downregulation of lncRNA HSD11B1-AS1 promotes proliferation, migration, and invasion of breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Unveiling histotype-specific biomarkers in ovarian carcinoma using proteomics.Molecular therapy. Oncology · 2025Article
- Regulator of chromosome condensation 1 promotes hepatocellular carcinoma proliferationWorld journal of gastrointestinal oncology · 2025Article
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- RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.The Journal of biological chemistry · 2024Article
- Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway.Thoracic cancer · 2023Article
- Lnc-HZ08 regulates BPDE-induced trophoblast cell dysfunctions by promoting PI3K ubiquitin degradation and is associated with miscarriage.Cell biology and toxicology · 2022Article
- Curcumin promotes cell cycle arrest and apoptosis of acute myeloid leukemia cells by inactivating AKT.Oncology reports · 2021Article
- Revealing the Potential Application of EC-Synthetic Retinoid Analogues in Anticancer Therapy.Molecules (Basel, Switzerland) · 2021Article
- Identification of a Genome Instability-Associated LncRNA Signature for Prognosis Prediction in Colon Cancer.Frontiers in genetics · 2021Article
- Correction to: Downregulation of GLYR1 contributes to microsatellite instability colorectal cancer by targeting p21 via the p38MAPK and PI3K/AKT pathways.Journal of experimental & clinical cancer research : CR · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundGLYR1 has a high mutation frequency in microsatellite instability colorectal cancer (MSI CRC) and is presumed to be a novel tumor suppressor. However, the role of GLYR1 in tumors has never been studied. In particular, the downregulation of GLYR1 in MSI CRC is worthy of further investigation.
methodsWestern blot and immunohistochemistry analyses were used to detect GLYR1 protein expression in CRC tissues and cell lines, and the clinical significance of GLYR1 was also analyzed. The relationship between GLYR1 and MLH1 was validated by immunofluorescence, immunoprecipitation and bioinformatics analyses. Western blotting, qRT-PCR, CCK-8 assays, colony formation assays, flow cytometry and Hoechst 33258 staining assays were used to assess the effect of GLYR1 on the cell cycle progression, proliferation, differentiation and apoptosis of CRC cells in vitro. The related mechanisms were initially investigated by Western blotting.
resultsGLYR1 was significantly downregulated in MSI CRC and its expression was negatively correlated with tumor size and positively correlated with tumor differentiation in CRC patients. In addition, GLYR1 interacted with MLH1 to regulate its nuclear import and expression. Moreover, downregulation of GLYR1 accelerated G1/S phase transition, promoted proliferation and inhibited differentiation of SW480 and SW620 cells in vitro. Furthermore, downregulation of GLYR1 decreased the sensitivity to 5-fluorouracil (5-FU) by inhibiting the mitochondrial apoptosis pathway in CRC cells. Inhibition of the p38 mitogen-activated protein kinase (p38MAPK) and activation of the phosphatidyl 3-kinase/protein kinase B (PI3K/Akt) signaling pathways were involved in the mechanism by which GLYR1 downregulated p21.
conclusionsOurs is the first study to elucidate the role of GLYR1 in tumors and provide evidence for GLYR1 as a biological marker that reflects the degree of malignancy and sensitivity to 5-FU in MSI CRC.
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