ALKBH5 promotes the progression of infantile hemangioma through regulating the NEAT1/miR-378b/FOSL1 axis

Peng, Kun; Xia, Renpeng; Zhao, Fan; Xiao, Yong; Ma, Ti-Dong; Li, Ming; Feng, Yong; Zhou, Chong-Gao

doi:10.1007/s11010-022-04388-2

Cited by 7 publications

(2 citation statements)

References 47 publications

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“…Recently, some studies have revealed that ALKBH5 detaches m 6 A modification on various LncRNAs and involves in the occurrence and development of various tumors [ 47 – 60 ]. As we all known, LncRNA nuclear enriched abundant transcript 1 (NEAT1) is a carcinogenic LncRNA and its level and function were closely related to ALKBH5-demethylated m 6 A modification [ 47 – 51 ] . Literature from Dong et al indicated that m 6 A-modified LncRNA NEAT1 was involved in glioblastoma multiforme.…”

Section: Lncrnas Regulated By M 6 a Modification I...mentioning

confidence: 99%

“…As same in gastric cancer, ALKBH5 also could up-regulate LncRNA NEAT1 expression by inhibiting m 6 A enrichment on LncRNA NEAT1 in hepatocellular carcinoma [ 49 ] and in colon cancer [ 50 ]. In addition to digestive system tumors, the elevation of LncRNA NEAT1 expression promoted by ALKBH5 demethylation is also observed in infantile hemangioma [ 51 ]. ALKBH5-mediated m 6 A modification on LncRNAs also plays a key role in the development of respiratory system tumors.…”

Section: Lncrnas Regulated By M 6 a Modification I...mentioning

confidence: 99%

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Novel insights into mutual regulation between N6-methyladenosine modification and LncRNAs in tumors

et al. 2023

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N6-methyladenosine (m6A), one of the most common RNA methylation modifications, has emerged in recent years as a new layer of the regulatory mechanism controlling gene expression in eukaryotes. As a reversible epigenetic modification, m6A not only occurs on mRNAs but also on Long non-coding RNAs (LncRNAs). As we all known, despite LncRNAs cannot encode proteins, they affect the expression of proteins by interacting with mRNAs or miRNAs, thus playing important roles in the occurrence and development of a variety of tumors. Up to now, it has been widely accepted that m6A modification on LncRNAs affects the fate of the corresponding LncRNAs. Interestingly, levels and functions of m6A modifications are also mediated by LncRNAs through affecting the m6A methyltransferases (METTL3, METTL14, WTAP, METTL16, etc.), demethylases (FTO, ALKBH5) and methyl-binding proteins (YTHDFs, YTHDCs, IGF2BPs, HNRNPs, etc.), which are collectively referred to as “m6A regulators”. In this review, we summarized the mutual regulation mechanisms between N6-methyladenosine modification and LncRNAs in cancer progression, metastasis, invasion and drug resistance. In detail, we focus on the specific mechanisms of m6A modification, which is mediated by methyltransferases and demethylases, involves in the regulation of LncRNA levels and functions in the first part. And section two intensively displays the mediation roles of LncRNAs in m6A modification via changing the regulatory proteins. At last part, we described the interaction effects between LncRNAs and methyl-binding proteins of m6A modification during various tumor occurrence and development.

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