<i>MEIS1</i> knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Mahmoudian, Reihaneh Alsadat; Bahadori, Bahareh; Rad, Abolfazl; Abbaszadegan, Mohammad Reza; Forghanifard, Mohammad Mahdi

doi:10.1002/mgg3.746

Cited by 12 publications

(8 citation statements)

References 45 publications

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“…We have recently reported that MEIS1 knockdown in KYSE-30 cells can induce expression of epithelial differentiation markers CDX2, and KRT4, while it can suppress the involved genes in EMT process including TWIST1, EGF [35]. In line with this report, our presented results in this study support the potential oncogenic role for MEIS1 in promoting mesenchymal/ stemness phenotype of ESCC.…”

Section: Discussionsupporting

confidence: 90%

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

et al. 2020

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Background: MEIS1 (Myeloid ecotropic viral integration site 1) as a homeobox (HOX) transcription factor plays regulatory roles in a variety of cellular processes including development, differentiation, survival, apoptosis and hematopoiesis, as well as stem cell regulation. Few studies have established pluripotency and self-renewal regulatory roles for MEIS1 in human esophageal squamous cell carcinoma (ESCC), and our aim in this study was to evaluate the functional correlation between MEIS1 and the stemness markers in ESCC patients and cell line KYSE-30. Methods: Expression pattern of MEIS1 and SALL4 gene expression was analyzed in different pathological features of ESCC patients. shRNA in retroviral vector was used for constantly silencing of MEIS1 mRNA in ESCC line (KYSE-30). Knockdown of MEIS1 gene and the expression pattern of selected stemness markers including SALL4, OCT4, BMI-1, HIWI, NANOG, PLK1, and KLF4 were evaluated using real-time PCR. Results: Significant correlations were observed between MEIS1 and stemness marker SALL4 in different early pathological features of ESCC including non-invaded tumors, and the tumors with primary stages of progression. Retroviral knockdown of MEIS1 in KYSE-30 cells caused a noteworthy underexpression of both MEIS1 and major involved markers in stemness state of the cells including SALL4, OCT4, BMI-1, HIWI and KLF4. Conclusions: The results highlight the important potential role of MEIS1 in modulating stemness properties of ESCCs and cells KYSE-30. These findings may confirm the linkage between MEIS1 and self-renewal capacity in ESCC and support probable oncogenic role for MEIS1 in the disease.

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Section: Discussionsupporting

confidence: 90%

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

et al. 2020

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“…The role of the whole MEIS protein family (MEIS1, MEIS2, and MEIS3) in solid cancers has been recently reviewed by Girgin and colleagues [105]. MEIS1 overexpression in several solid cancers has an important oncogenic function, for example, in breast [106,107], colorectal [108], human esophageal squamous cell [109,110], neuroblastoma [111], ovarian [112], and prostate cancers [113], where its upregulation has been associated to cancer etiology, progression, and increased invasiveness.…”

Section: The Role Of Meis1 In Solid Cancersmentioning

confidence: 99%

MEIS1 in Hematopoiesis and Cancer. How MEIS1-PBX Interaction Can Be Used in Therapy

Blasi

Bruckmann

2021

JDB

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Recently MEIS1 emerged as a major determinant of the MLL-r leukemic phenotype. The latest and most efficient drugs effectively decrease the levels of MEIS1 in cancer cells. Together with an overview of the latest drugs developed to target MEIS1 in MLL-r leukemia, we review, in detail, the role of MEIS1 in embryonic and adult hematopoiesis and suggest how a more profound knowledge of MEIS1 biochemistry can be used to design potent and effective drugs against MLL-r leukemia. In addition, we present data showing that the interaction between MEIS1 and PBX1 can be blocked efficiently and might represent a new avenue in anti-MLL-r and anti-leukemic therapy.

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“… 13 MEIS1 has a key role in the regulation of the stemness state of stem cells and the transcription adjustment of self-renewal genes, as well as involved genes in cell development and differentiation, playing an oncogenic role in several tumors. 21 It has been reported that ELF1 can act as an important positive transcriptional regulator of the Hox cofactor MEIS1. 16 Therefore, we hypothesized that ELF1 may affect glioma development by regulating the transcription of MEIS1.…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor ELF1 Activates MEIS1 Transcription and Then Regulates the GFI1/FBW7 Axis to Promote the Development of Glioma

Cheng

Zeng

Zhang

et al. 2021

Molecular Therapy - Nucleic Acids

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Glioma is the most common malignancy in the central nervous system with no immediate prospect of a cure. Comprehensive understanding on the pathogenesis of the disorder contributes to a better outcome. Herein, we aimed to investigate whether transcription factors erythroblast transformation-specific (ETS) transcription factor (ELF1), myeloid ecotropic viral integration site 1 (MEIS1), and growth factor independence 1 (GFI1)/F-box/WD repeat-containing protein 7 (FBW7) mediate progression of glioma. ELF1, MEIS1, and GFI1 were upregulated in glioma cells and tissues, as ELF1 was correlated with poor prognosis. Bioinformatics analysis identified the binding between ELF1 and MEIS1 as well as between GFI1 and FBW7, confirmed by chromatin immunoprecipitation (ChIP) experiments. Functional experiment indicated that silencing of ELT1 decreased MEIS1 expression and that overexpression of MEIS1 increased GFI1 expression by activating GFI1 enhancer but decreased FBW7 expression. Importantly, silencing of ELF1 decreased the capacities of proliferation, migration, and invasion of glioma cells whereas it increased apoptosis, supported by increased capase-3 and decreased matrix metalloproteinase-9 (MMP-9) and proliferating cell nuclear antigen (PCNA) expression. Moreover, an in vivo experiment confirmed the inhibitory role of silenced ELF1 in tumor growth, with a decreased level of MEIS1 and GFI1. Taken together, our study elucidated a potential mechanism that ELF1 promoted cell progression by increasing GFI1 and METS1 as well as decreasing FBW7 expression in glioma.

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MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Cited by 12 publications

References 45 publications

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

MEIS1 promotes expression of stem cell markers in esophageal squamous cell carcinoma

MEIS1 in Hematopoiesis and Cancer. How MEIS1-PBX Interaction Can Be Used in Therapy

Transcription Factor ELF1 Activates MEIS1 Transcription and Then Regulates the GFI1/FBW7 Axis to Promote the Development of Glioma

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