ArticleMolecular and cellular biochemistry2019
Activation of EMT in colorectal cancer by MTDH/NF-κB p65 pathway.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Metadherin: A pivotal oncogene and therapeutic target in head and neck cancer - a systematic review.The Japanese dental science review · 2026Review
- LDLRAD2 drives glycolysis and angiogenesis to promote extramedullary infiltration in acute myeloid leukemia.iScience · 2026Article
- Recent Advancements in Drug Targeting for Ferroptosis as an Antitumor Therapy: Development of Novel therapeutics.Current cancer drug targets · 2026Review
- Rewiring tumor immunity via zinc finger proteins: a new frontier in cancer immunotherapy.Journal of translational medicine · 2025Review
- The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025Review
- Ferroptosis is an effective strategy for cancer therapy.Medical oncology (Northwood, London, England) · 2024Review
- Bioinformatic analysis reveals an association between Metadherin with breast cancer prognosis and tumor immune infiltration.Scientific reports · 2024Article
- The RioK1 network determines p53 activity at multiple levels.Cell death discovery · 2023Article
- CXCL14 promotes metastasis of non-small cell lung cancer through ACKR2-depended signaling pathway.International journal of biological sciences · 2023Article
- Calebin A targets the HIF-1α/NF-κB pathway to suppress colorectal cancer cell migration.Frontiers in pharmacology · 2023Article
- miR-217-5p suppresses epithelial-mesenchymal transition and the NF-κB signaling pathway in breast cancer via targeting of metadherin.Oncology letters · 2022Article
- Targeting Ferroptosis Pathway to Combat Therapy Resistance and Metastasis of Cancer.Frontiers in pharmacology · 2022Review
- The Expression, Prognostic Value, and Immunological Correlation of MCEMP1 and its Potential Role in Gastric Cancer.Journal of oncology · 2022Article
- Ketamine Induced Bladder Fibrosis Through MTDH/P38 MAPK/EMT Pathway.Frontiers in pharmacology · 2021Article
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- Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells by Regulating NOX2-ROS-Mediated Pro-Survival Signal Pathways.Drug design, development and therapy · 2020Article
- Metadherin enhances vulnerability of cancer cells to ferroptosis.Cell death & disease · 2019Article
- Period 2 Suppresses the Malignant Cellular Behaviors of Colorectal Cancer Through the Epithelial-Mesenchymal Transformation Process.Cancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) leads to tumor dissemination and metastasis. Metadherin (MTDH) is an oncogene that plays an important role in metastasis regulation. This study tries to investigate the effect of MTDH gene up-regulation on the activation of EMT in colorectal cancer (CRC) cells and identify the role of NF-κB p65. The CaCO2 cells were divided into three groups: one control group of cultured CaCO2 cells (C1), and two groups of CaCO2 cells co-transfected using human MTDH expression plasmid with either siRNA targeting human NF-κB p65 or its negative control (C2 and C3 respectively). The gene modification was confirmed by qPCR and the effect of gene modification on CRC aggravation was studied. MTDH up-regulation significantly promoted CRC cell proliferation, activated anaerobic respiration (glucose consumption and lactate production), and increased gene expression of multidrug resistance gene (MDR1), Snail transcription factor and NF-κB p65, but decreased the gene expression of E-cadherin. Moreover, MTDH up-regulation led to a significant increase in the acquisition of surface markers of CRC stem cells. Interference with NF-κB p65 gene expression reversed the action of MTDH gene up-regulation on MDR1 and E-cadherin gene expression and anaerobic respiration. Moreover, NF-κB p65 interference significantly decreased MTDH-induced cell proliferation and acquisition of surface markers of CRC stem cells but didn't affect the Snail transcription factor. MTDH-dependent EMT in CRC is activated via NF-κB p65 and is mediated by up-regulation of Snail. These results identify a pathway by which MTDH regulates NF-κB p65 induced EMT during CRC cell metastasis.
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