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It is well known that RNA methylation-related enzymes are comprehensive in function and play a key role in the development of various cancer diseases. The same enzyme works in different cancers in the opposite direction! For example, METTL14 is an anti-cancer guardian in glioma GBM and liver cancer HCC. It can be turned into an oncogene in acute leukemia AML, and the change is amazing. Although the methylation modification sites are various and have different functions, they eventually cause changes in the phenotype of cancer cells. I believe that in the next basic research, RNA methylase Writer and demethylase Eraser Recognition of protein Reader is still the most important.
1.The function of m6A related enzymes in cancer
The functions of methyltransferases (METTL3 and METTL14), demethylases (NSun2, FTO and ALKBH5) and reading enzymes (YTHDF2) in various cancers are summarized below. 
2. Molecular mechanism of m6A in cancer
Next, we will introduce the important functions of m6A RNA methylation in regulating the differentiation, proliferation, migration and immunity of cancer stem cells. 
1) Hematopoietic stem cells (HSCs) are often used as an ideal model for studying the differentiation process because of the easy to detect differentiation state. The most prominent feature of myeloid hematological malignancies is the abnormal differentiation state. Recent studies have shown that METTL3 expression is significantly up-regulated in leukemia cells compared to normal hematopoietic stem cells, and METTL3 can up-regulate methylation levels of target genes including MYC, BCL2, and PTEN in the leukemia cell line MOLM-13, thereby promoting these Translation of gene expression. This study also showed that METTL3 can regulate gene translation levels in cells by m6A methylation to maintain pluripotency and inhibit cell differentiation. Inhibition of METTL3 in human leukemia cell lines can mediate cell differentiation and apoptosis and delay the progression of leukemia. Consistent with METTL3, METTL14 is also highly expressed in AML cells carrying t(11q23) t(15;17) chromosomal abnormalities. METTL14 can also exert cancer-promoting effects through its target genes (eg MYB MYC, etc.), but METTL14 The enzyme protein itself is negatively regulated by the SPI1 gene. This upstream and downstream regulation axis SPI1/METTL14/MYB and MYC jointly regulate the development of leukemia. In addition, another RNA methylase complex member, RMB15, and the m6A recognition protein WTAP are also highly correlated with the development of myeloid leukemia.
An increase in m6A methylation levels in certain disease environments can inhibit stem cell proliferation. Some studies have shown that R-2HG exhibits extensive proliferation inhibition in leukemia cells. R-2HG upregulates m6A methylation by inhibiting FTO, so R-2HG/FTO/MYC and CEBPA regulatory axes can be found in leukocyte environments. Play an important regulatory function.
2) On the other hand, the down-regulation of m6A RNA methylation may play a role in promoting cancer. For example, FTO can promote leukemia protooncogene-mediated cell transformation and inhibit ATRA-mediated leukemia cell differentiation. FTO exerts a cancer-promoting effect by down-regulating the methylation level of m6A of target genes (such as ASB2, RARA, etc.). RNA stability analysis showed that the effect of FTO on ASB2 and RARA was partly due to the stability of mRNA affecting ASB2 and RARA, thus demonstrating that FTO/ASB2 and RARA axes play an important role in the pathogenesis of AML.
2.2 m6A methylation is associated with cancer cell proliferation 
1) m6A is involved in a variety of cancer cell proliferation processes. There is a close relationship between HBXIP and METTL3 in the progression of breast cancer BC. HBXIP can up-regulate METTL3 by inhibiting miRNA let-7g, while METTL3 can up-regulate the expression of HBXIP through m6A modification, forming HBXIP/let-7g/METTL3/HBXIP. A positive feedback regulation mode that accelerates cell proliferation in breast cancer. Taking human liver cancer (HCC) as an example, the expression of up-regulated METTL3 regulates the progression of HCC in a special way. SOCS2 in the SOC family is a tumor suppressor gene that negatively regulates the JAK/STAT signaling pathway, and it is expected that METTL3 can up-regulate the m6A methylation level of SOCS2 mRNA and degrade its mRNA by relying on YTHDF2, thereby reducing SOCS2. The amount of expression.
2.3 m6A RNA methylation enhances migration and metastasis of cancer cells 
1) Among the transferable HCC, METTL3 regulated m6A modification can affect DGCR8 on pri-miRNA processing. METTL14 can also affect the processing and maturation of pri-miRNA by regulating the process of DGCR8 recognition or binding to pri-miRNA. Experiments show that knockdown of METTL14 leads to processing stagnation of pri-miR126, down-regulation of mature miR126 expression, and miR126 is a tumor. The important inhibitory molecule of metastasis, down-regulation of miR126 expression, can lead to an increase in tumor cell metastatic ability.
2) Among colorectal cancers (CRC), serine proteases are important members of the tumor microenvironment, and they can selectively activate PAR2 receptors by proteolysis. Studies have shown that PAR2 activation can reduce the expression of miR-125b by NSun2, which can methylate miR-125b precursor molecule pre-miR-125b to interfere with the maturation process of this molecule, thereby reducing the expression of mature miR-125b. . Down-regulation of miR-125b expression leads to an increase in its target gene Gab2, which greatly enhances cell migration ability.
3) Among human pancreatic cancers (PC), YTHDF2 is significantly increased in both mRNA and protein levels, and YTHDF2 regulates cell proliferation and transition from epithelial to mesenchymal cells (EMT). YTHDF2 regulates cell proliferation and EMT via the Akt/GSK3b/CYclinD1 pathway and inhibits migration, invasion, and adhesion.
2.4 m6A participates in the tumor immune process 
The initial literature reported that m6A methylation is involved in the regulation of T cell homeostasis by targeting the IL-7/STAT5/SOCS axis. Toll-like receptors (TLRs) are the most conserved molecules in the endogenous immune system and are the first line of defense against pathogens. RNA molecules with m6A methylation modification cannot activate partial TLR molecules. This process leads to the inability of TLR receptors to recognize some pathogens including viral nucleic acids. M6A methylation also affects the base pairing process, thus m6A enables RNA. The complex is unstable, which explains why RNA molecules with m6A modification cannot activate TLR3. Compared to unmodified RNA molecules, m6A-modified RNA molecules allow dendritic DCs to express less cytokines and activating factors. The viral components that have escaped the first defense system further activate cancer-related signaling pathways that cause cancer to develop.
to sum up
The role of RNA methylase and RNA methylation in a variety of diseases has been reported. In this paper, the latest enzymes of RNA-integrated RNA methylation and RNA methylation in cancer and cancer stem cells are studied. , Cloud Presence Bio suggests that more researchers choose to focus on RNA methylation-related enzymes and RNA methylation studies in different pathophysiological contexts, then how to quickly and simultaneously detect RNA methylation-related enzymes & RNA methylation, cloud The sequence organism recommends a shortcut, and at the same time, RNA-seq&m6A-seq is used to quickly find the whereabouts of various important enzymes in the RNA-seq data, lock in the expression changes, and then integrate the m6A-seq data to start the enzyme. The level of methylation is then found at the RNA-seq level for gene expression. m6A-seq&RNA-seq is a one-stop process that demonstrates cost-effectiveness, both the detection of RNA methylation levels and the detection of transcriptome levels, as well as changes in upstream RNA methylases. For more detailed solutions, you can call our professional technicians. In the next issue of the public number, we will specifically explain how to start from the enzyme, study the role of enzymes in different disease backgrounds, and publish a high-quality RNA methylation research article.
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How to quickly and simultaneously detect RNA methylation-related enzymes & RNA methylation levels in various cancers
Occupy C! How does cloud-sequence bioanalysis quickly and simultaneously detect RNA methylation-related enzymes & RNA methylation levels in various cancers
As the main research product of cloud-sequence organisms, RNA methylation has helped many research teams to carry out RNA methylation research. As a leader in domestic RNA methylation research, Yunxu Bio is a mature service provider of domestic RNA methylation 10 points. It launched the non-coding RNA methylation sequencing research and launched the ultra-micro RNA methylation. Sequencing technology, the first launch of a one-stop systemic solution for RNA methylation research, Cloud Sequence brings the latest RNA to the researchers in the New Year's opening with the M6A RNA methylation in cancer. A summary of studies on methylation-related enzymes in cancer. This article is intended to emphasize the importance of RNA methylase research, and to provide you with mature RNA methylation research ideas, how to study, how to study is the cloud sequence has long been a question for everyone to answer.
Table 1. Function of m6A RNA methylation modification in various cancers
2.1 RNA methylase and cancer stem cell (CSC) pluripotency related to cell differentiation