2010 June | Bríd M. Ryan, Ana I. Robles, and Curtis C. Harris
The article discusses the role of microRNA (miRNA) genetic variations in cancer research. It highlights how single nucleotide polymorphisms (SNPs) in miRNA genes, their processing machinery, and target binding sites can influence cancer risk, treatment response, and prognosis. The review outlines the methods used to study these variations and suggests future research directions.
Human populations are 99% genetically identical, with the remaining 1% due to SNPs, which are non-repetitive sequence variations. Over 10 million SNPs have been identified in the human genome, with many linked to cancer risk through gene-environment interactions. miRNAs, a class of non-coding RNAs, regulate gene expression by binding to mRNA. Recent studies show that miRNA SNPs can affect miRNA function, and their association with cancer risk has been supported by case-control studies.
miRNA SNPs can affect function through transcription of primary transcripts, processing of pre-miRNAs, or miRNA-mRNA interactions. Functional studies have shown that SNPs in miRNA genes can influence miRNA expression and cancer susceptibility. For example, a germline mutation in pri-mir-16-1 was linked to chronic lymphocytic leukaemia. SNPs in miRNA binding sites can create or destroy miRNA binding sites, affecting gene expression.
Several miRNA SNPs have been associated with cancer risk, including those in miRNA genes and miRNA binding sites. For instance, rs7372209 in mir-26a-1 was linked to reduced bladder cancer risk in females. SNPs in miRNA processing machinery, such as DROSHA and DICER1, may affect miRNA maturation and cancer risk, though their biological mechanisms remain unclear.
IsomiRs, variations in miRNA sequences, have been identified and may influence miRNA function. Some isomiRs are associated with cancer, but their role in disease is not fully understood. miRNA expression can also be affected by epigenetic factors, such as DNA methylation, which may influence cancer susceptibility.
The review emphasizes the importance of studying miRNA genetic variations in cancer research, highlighting the need for further validation of SNPs and their functional impact. It also suggests that future studies should consider the complex interactions within miRNA networks and the role of miRNA processing in cancer development. The integration of miRNA target co-expression and expression Quantitative Trait Locus (eQTL) mapping could help determine the functional significance of miRNA SNPs. Overall, the study underscores the significance of miRNA genetic variations in cancer susceptibility and the need for further research to fully understand their role in disease.The article discusses the role of microRNA (miRNA) genetic variations in cancer research. It highlights how single nucleotide polymorphisms (SNPs) in miRNA genes, their processing machinery, and target binding sites can influence cancer risk, treatment response, and prognosis. The review outlines the methods used to study these variations and suggests future research directions.
Human populations are 99% genetically identical, with the remaining 1% due to SNPs, which are non-repetitive sequence variations. Over 10 million SNPs have been identified in the human genome, with many linked to cancer risk through gene-environment interactions. miRNAs, a class of non-coding RNAs, regulate gene expression by binding to mRNA. Recent studies show that miRNA SNPs can affect miRNA function, and their association with cancer risk has been supported by case-control studies.
miRNA SNPs can affect function through transcription of primary transcripts, processing of pre-miRNAs, or miRNA-mRNA interactions. Functional studies have shown that SNPs in miRNA genes can influence miRNA expression and cancer susceptibility. For example, a germline mutation in pri-mir-16-1 was linked to chronic lymphocytic leukaemia. SNPs in miRNA binding sites can create or destroy miRNA binding sites, affecting gene expression.
Several miRNA SNPs have been associated with cancer risk, including those in miRNA genes and miRNA binding sites. For instance, rs7372209 in mir-26a-1 was linked to reduced bladder cancer risk in females. SNPs in miRNA processing machinery, such as DROSHA and DICER1, may affect miRNA maturation and cancer risk, though their biological mechanisms remain unclear.
IsomiRs, variations in miRNA sequences, have been identified and may influence miRNA function. Some isomiRs are associated with cancer, but their role in disease is not fully understood. miRNA expression can also be affected by epigenetic factors, such as DNA methylation, which may influence cancer susceptibility.
The review emphasizes the importance of studying miRNA genetic variations in cancer research, highlighting the need for further validation of SNPs and their functional impact. It also suggests that future studies should consider the complex interactions within miRNA networks and the role of miRNA processing in cancer development. The integration of miRNA target co-expression and expression Quantitative Trait Locus (eQTL) mapping could help determine the functional significance of miRNA SNPs. Overall, the study underscores the significance of miRNA genetic variations in cancer susceptibility and the need for further research to fully understand their role in disease.