ReviewFrontiers in oncology2025
Interactions between ALKBH5 and reader proteins in tumors: functions and molecular mechanisms.
Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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8 authors.
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Abstract
RNA methylation modifications are widespread in eukaryotes and prokaryotes, with N6-methyladenosine (m6A) methylation being the most prevalent internal modification in eukaryotic mRNA and having become a prominent focus of tumor research in recent years. Up to now, substantial evidence has suggested that the dysregulated RNA demethylase ALKBH5 can interact with m6A reader proteins to modulate a wide range of mRNA biological progress, including mRNA shearing, export, metabolism, and stability, ultimately influencing tumorigenesis and development. To deeply understand the regulatory roles of ALKBH5 and reader proteins in tumor progression, this review aims to summarize the structures of ALKBH5 and reader proteins, as well as their cooperative regulatory mechanisms that affect the occurrence and development of tumors originating from different systems. Furthermore, the potential applications of targeting ALKBH5 and reader proteins in antitumor drug development are summarized, hoping to provide a strong basis for advancing antineoplastic research in the future.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.