Dysregulation of Non-Coding RNAs: Roles of miRNAs and lncRNAs in the Pathogenesis of Multiple Myeloma.
Nor Hayati IsmailAli MussaMutaz Jamal Al-KhreisatShafini Mohamed YusoffAzlan HusinHamid Ali Nagi Al-JamalMuhammad Farid JohanMd Asiful IslamPublished in: Non-coding RNA (2023)
The dysregulation of non-coding RNAs (ncRNAs), specifically microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), leads to the development and advancement of multiple myeloma (MM). miRNAs, in particular, are paramount in post-transcriptional gene regulation, promoting mRNA degradation and translational inhibition. As a result, miRNAs can serve as oncogenes or tumor suppressors depending on the target genes. In MM, miRNA disruption could result in abnormal gene expression responsible for cell growth, apoptosis, and other biological processes pertinent to cancer development. The dysregulated miRNAs inhibit the activity of tumor suppressor genes, contributing to disease progression. Nonetheless, several miRNAs are downregulated in MM and have been identified as gene regulators implicated in extracellular matrix remodeling and cell adhesion. miRNA depletion potentially facilitates the tumor advancement and resistance of therapeutic drugs. Additionally, lncRNAs are key regulators of numerous cellular processes, such as gene expression, chromatin remodeling, protein trafficking, and recently linked MM development. The lncRNAs are uniquely expressed and influence gene expression that supports MM growth, in addition to facilitating cellular proliferation and viability via multiple molecular pathways. miRNA and lncRNA alterations potentially result in anomalous gene expression and interfere with the regular functioning of MM. Thus, this review aims to highlight the dysregulation of these ncRNAs, which engender novel therapeutic modalities for the treatment of MM.
Keyphrases
- gene expression
- genome wide identification
- dna methylation
- long non coding rna
- transcription factor
- multiple myeloma
- genome wide
- genome wide analysis
- extracellular matrix
- cell adhesion
- network analysis
- oxidative stress
- signaling pathway
- poor prognosis
- endoplasmic reticulum stress
- squamous cell carcinoma
- copy number
- dna damage
- small molecule
- heat shock protein