ArticleMolecular genetics & genomic medicine2019
MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE-30.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Down-regulation of circ0001361 induces apoptosis and suppresses the progression of glioma.PloS one · 2026Article
- The impact ofAnimal cells and systems · 2024Article
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- MEIS1 in Hematopoiesis and Cancer. How MEIS1-PBX Interaction Can Be Used in Therapy.Journal of developmental biology · 2021Review
- MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021Review
- Crosstalk between MMP-13, CD44, and TWIST1 and its role in regulation of EMT in patients with esophageal squamous cell carcinoma.Molecular and cellular biochemistry · 2021Article
- Correlation between the immune checkpoints and EMT genes proposes potential prognostic and therapeutic targets in ESCC.Journal of molecular histology · 2021Article
- Transcription Factor ELF1 Activates MEIS1 Transcription and Then Regulates the GFI1/FBW7 Axis to Promote the Development of Glioma.Molecular therapy. Nucleic acids · 2021Article
- MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma.BMC cancer · 2020Article
- Crosstalk between MEIS1 and markers of different cell signaling pathways in esophageal squamous cell carcinoma.Molecular biology reports · 2020Article
- MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE-30.Molecular genetics & genomic medicine · 2019Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMEIS1 (Myeloid ecotropic viral integration site 1), as a homeobox (HOX) transcription factor, has a dual function in different types of cancer. Although numerous roles are proposed for MEIS1 in differentiation, stem cell function, gastrointestinal development and tumorigenesis, the involved molecular mechanisms are poor understood. Our aim in this study was to elucidate the functional correlation between MEIS1, as regulator of differentiation process, and the involved genes in cell differentiation in human esophageal squamous carcinoma (ESC) cell line KYSE-30.
methodsThe KYSE-30 cells were transduced using recombinant retroviral particles containing specific shRNA sequence against MEIS1 to knockdown MEIS1 gene expression. Following RNA extraction and cDNA synthesis, mRNA expression of MEIS1 and the selected genes including TWIST1, EGF, CDX2, and KRT4 was examined using relative comparative real-time PCR.
resultsRetroviral transduction caused a significant underexpression of MEIS1 in GFP-hMEIS1 compared to control GFP cells approximately 5.5-fold. While knockdown of MEIS1 expression caused a significant decrease in EGF and TWIST1 mRNA expression, nearly -8- and -12-fold respectively, it caused a significant increase in mRNA expression of differentiation markers including KRT4 and CDX2, approximately 34- and 1.14-fold, correspondingly.
conclusionMEIS1 gene silencing in KYSE-30 cells increased expression of epithelial markers and decreased expression of epithelial-mesenchymal transition (EMT) marker TWIST1. It may highlight the role of MEIS1 in differentiation process of KYSE-30 cells. These results may confirm that MEIS1 silencing promotes differentiation and decreases EMT capability of ESC cell line KYSE-30.
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