MECOM Gene Editing    

The MDS1 and EVI1 complex locus protein (MECOM) gene is located on chromosome 3q26 and encodes a zinc-finger protein as a transcriptional regulator of hematopoietic stem cell self-renewal and long-term activity. MECOM (3q26) was originally identified as a common ecotropic viral integration site 1 (Evi1), which is common in murine myeloid leukemia. Its isoforms act as transcription factors. They contain an N-terminal (ZF1) and C-terminal (ZF2) zinc finger domain composed of seven and three C2H2-type zinc finger motifs, respectively. Evi1 is involved in the maintenance and differentiation of hematopoietic stem cells and the occurrence of leukemia. Overexpression of the MECOM gene in hematopoietic progenitors induces a myeloid differentiation block, leading to increased self-renewal and survival of these transformed progenitors.

Figure 1. MECOM C₂H₂-type zinc finger motif 9. (Ripperger T, et al., 2018)

MECOM can encode EVI1 and MDS1-EVI1 proteins (PRDM3). MECOM is essential for early development, hematopoiesis, proliferation, and cell differentiation. Studies have shown that PRDM3 has an important role in neurogenesis and craniofacial development. In addition, deletion of MECOM causes craniofacial defects and neuronal differentiation deficiency. The function and promoter activity of PRDM3 (MDS1-EVI) in the hematopoietic system has been described in detail. Meanwhile, MECOM is a known oncogene, which can regulate differentiation, proliferation and apoptosis of tumorigenesis. Abnormally high expression of MECOM has strong oncogenic properties. Amplification and overexpression of MECOM have been discovered in renal cell carcinoma and ovarian cancer. Increased MECOM expression in acute and chronic myeloid leukemia is associated with poor patient survival. MECOM is a regulator of stomach-specific genes, some of which are upregulated in dedifferentiated acinar cells, and was identified in a specific cluster of acinar cells during PDAC development in a recently published scRNAseq experiment. Earlier, a role for MECOM in pancreas cancer was proposed.

It is reported that MECOM gene overexpression occurs in about 8–15% of pediatric patients with acute myeloid leukemia (AML) and has been associated with an adverse prognosis in both adult and pediatric myeloproliferative neoplasms. Thus, assessment of MECOM gene expression, in addition to other known molecular and cytogenetic abnormalities, can provide a wider biological landscape and further clinical information, which will contribute to the application of a better risk stratified therapy, especially in patients with AML that lack other known genetic abnormalities.

MECOM Gene Editing Services

CRISPR/Cas9 Platform^CB at Creative Biogene is dedicated to offering comprehensive CRISPR/Cas9 gene editing services and products for academic research, biotech research and pharmaceutical drug discovery. With deep gene editing knowledge and extensive experience in experimental operation and data processing, we help you effectively control MECOM genes knockout/knockin/point mutation in cells or animals via CRISPR/Cas9 technology.

Service	Details	Alternative cell lines or animal species
MECOM Gene Editing Cell Line Generation	gRNA design and synthesis Transfect the cell lines you're interested Select the high expression cells and sort monoclonal cell Validate the knockout/knockin/point mutation of MECOM by PCR and sequencing Provide cryogenically preserved vials of stable cells and final reports	HEK239T, Hela, HepG2, U87, Ba/F3, CHO, MDA-MB-453, MDA-MB-231NIH3T3, T47D, Neuro2a, MCF7, RKO, K562, RAW264.7, etc.
MECOM Gene Editing Animal Model Generation	MECOM gene conventional knockout animals MECOM gene conditional knockout animals MECOM point mutation animals MECOM knockin animals	Mouse, rat, rabbit, zebrafish, C. elegans, etc.

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