Highlighting the role of long non-coding RNA (LncRNA) in multiple myeloma (MM) pathogenesis and response to therapy

Transcripts longer than 200 nucleotides that are not translated into proteins are known as long non-coding RNAs, or lncRNAs. Now, they are becoming more significant as important regulators of gene expression, and as a result, of many biological processes in both healthy and pathological circumstance...

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Veröffentlicht in:Medical oncology (Northwood, London, England) London, England), 2024-06, Vol.41 (7), p.171, Article 171
Hauptverfasser: Al-Hawary, Sulieman Ibraheem Shelash, Jasim, Saade Abdalkareem, Altalbawy, Farag M. A., Hjazi, Ahmed, Jyothi, S. Renuka, Kumar, Ashwani, Eldesoqui, Mamdouh, Rasulova, M. T., Sinha, Aashna, Zwamel, Ahmed Hussein
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Sprache:eng
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Zusammenfassung:Transcripts longer than 200 nucleotides that are not translated into proteins are known as long non-coding RNAs, or lncRNAs. Now, they are becoming more significant as important regulators of gene expression, and as a result, of many biological processes in both healthy and pathological circumstances, such as blood malignancies. Through controlling alternative splicing, transcription, and translation at the post-transcriptional level, lncRNAs have an impact on the expression of genes. In multiple myeloma (MM), the majority of lncRNAs is elevated and promotes the proliferation, adhesion, drug resistance and invasion of MM cells by blocking apoptosis and altering the tumor microenvironment (TME). To control mRNA splicing, stability, and translation, they either directly attach to the target mRNA or transfer RNA-binding proteins (RBPs). By expressing certain miRNA-binding sites that function as competitive endogenous RNAs (ceRNAs), most lncRNAs mimic the actions of miRNAs. Here, we highlight lncRNAs role in the MM pathogenesis with emphasize on their capacity to control the molecular mechanisms known as “hallmarks of cancer,” which permit earlier tumor initiation and progression and malignant cell transformation.
ISSN:1559-131X
1357-0560
1559-131X
DOI:10.1007/s12032-024-02392-8