![]() VM is a new tumor microcirculation model the blood vessels formed in VM can transport sufficient nutrients and blood supply to support tumor growth. In addition to traditional tumor angiogenesis, vasculogenic mimicry (VM), which is independent of endothelial cells, was first described as a novel process by Maniotis et al. To meet the demands caused by their growth and development, tumors need to form new blood vessels to transport nutrients and oxygen. Therefore, it is essential to understand how CRC develops and identify therapeutic targets to improve patient prognosis. Although many studies have clarified the biological characteristics of CRC, morbidity and mortality remain high among patients with this type of cancer. The identification of prognostic and predictive biomarkers for early diagnosis, prevention, and targeted therapy is a major challenge for CRC researchers. The study suggests that intervention with m6A-binding proteins (METT元 and IGF2BP2/3) may provide a potential diagnostic or prognostic target of VM-based anti-metastasis drugs for CRC.Ĭolorectal cancer (CRC) is among the 10 most common cancers worldwide, ranking third for incidence, but second for mortality, and the incidence rate is rising worldwide. In addition, EphA2 and VEGFA targeted by METT元 via different IGF2BP-dependent mechanisms were found to promote vasculogenic mimicry (VM) formation via PI3K/AKT/mTOR and ERK1/2 signaling in CRC. The results in vitro revealed that METT元 as the m6A “writers” participates the methylation of EphA2 and VEGFA, which were recognized by the m6A “readers”, insulin-like growth factor 2 mRNA binding protein 2/3 (IGF2BP2/3), to prevent their mRNA degradation. Moreover, transcriptome sequencing in METT元 knockdown cells using CRISPR/Cas9 editing suggested that EphA2 and VEGFA were differential expression, which were enriched in the vasculature development, PI3K/AKT and ERK1/2 signal pathway through the functional enrichment analysis. Analysis using high-throughput RNA-seq profile from TCGA found that the gene expression of Methyltransferase-like 3 (METT元) was significantly upregulated among 20 m6A binding proteins in CRC, which was also validated in CRC cancer tissues and cell lines. Exploring the epigenetic regulation mechanism of colorectal cancer (CRC) from the perspective of N6-methyladenosine (m6A) modification may provide a new target for tumor therapy. ![]()
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