ArticleFrontiers in genetics2025
A novel mechanism by which c-MYC is aberrantly activated by epigenetic silencing of its antisense lncRNA in colon cancer.
Article in Frontiers in genetics, 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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Abstract
Background: Proto-oncogenes are abnormally activated in nearly all types of tumors. However, the epigenetic mechanism of proto-oncogene activation has not yet been well elucidated. Methods: The present study involved the construction of a double-stranded cDNA library derived from gastrointestinal cancer cells, followed by high-throughput genome sequencing to select the c-MYC gene associated with colorectal cancer. Through RACE analysis, we identified the antisense RNA MYC-AS1 and its complete sequence. By investigating the cellular functions, expression of MYC-AS1, elucidating its interaction mechanism with the c-MYC gene, and exploring the impact of DNA methylation on MYC-AS1 expression, we uncover the fundamental principles and regulatory mechanisms underlying colorectal cancer development. Results: Here, we show that a subset of proto-oncogenes,including c-MYC, possess antisense RNAs. Upregulation of c-MYC in cancer tissues was attributed to the silencing of its antisense RNA MYC-AS1 via DNA hypermethylation. MYC-AS1 RNA markedly inhibited the proliferation of cancer cells in vitro and impeded tumor growth in nude mice in vivo by repressing the expression of c-MYC via an RNAi mechanism. MYC-AS1 RNA bound directly to the HuR protein in the cytoplasm, enhancing the RNA stability of MYC-AS1. Furthermore, MYC-AS1 inhibited c-MYC-targeted gene LDHA expression. Unlike the well-characterized oncogenic long noncoding RNA PVT1, which is coamplified with MYC and enhances its stability, MYC-AS1 is epigenetically silenced and functions as a tumor suppressor through an RNAi mechanism, revealing a distinct layer of MYC regulation. Conclusion: Our work provides a novel mechanism by which c-MYC is activated in cancer cells by epigenetic silencing of its antisense RNA, which functions as a tumor suppressor.
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