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- W2894310390 abstract "TNR expansions can be the cause of neurological disorders. Multiple mechanisms have been described to explain the pathology. A major goal in the field has been to target TNR-containing genes to reduce pathology. Usually, genes are targeted outside their TNR. While TNR diseases can have devastating consequences for affected patients, CAG-based TNR diseases in particular have reduced cancer load. Many TNR-containing RNAs can be transcribed and give rise to small RNAi-active RNAs. TNR-derived siRNAs kill cancer cells by targeting reverse complementary TNR stretches. Many genes in most genomes of higher organisms contain TNRs longer than 18 nt. They can be located in any gene element. Analysis of diseases that have reduced cancer load may result in the identification of novel anticancer mechanisms that could be exploited for cancer treatment. Many neurodegenerative diseases are caused by unstable trinucleotide repeat (TNR) expansions located in disease-associated genes. siRNAs based on CAG repeat expansions effectively kill cancer cell lines in vitro through RNAi. They also cause significant reduction in tumor growth in a human ovarian cancer mouse model with no toxicity to the treated mice. This suggests that cancer cells are particularly sensitive to CAG TNR-derived siRNAs, and explains a reported inverse correlation between the length of CAG TNRs and reduced global cancer incidences in some CAG TNR diseases. This review discusses both mutant proteins and mutant RNAs as a cause of TNR diseases, with a focus on RNAi and its role in contributing to disease pathology and in suppressing cancer. Many neurodegenerative diseases are caused by unstable trinucleotide repeat (TNR) expansions located in disease-associated genes. siRNAs based on CAG repeat expansions effectively kill cancer cell lines in vitro through RNAi. They also cause significant reduction in tumor growth in a human ovarian cancer mouse model with no toxicity to the treated mice. This suggests that cancer cells are particularly sensitive to CAG TNR-derived siRNAs, and explains a reported inverse correlation between the length of CAG TNRs and reduced global cancer incidences in some CAG TNR diseases. This review discusses both mutant proteins and mutant RNAs as a cause of TNR diseases, with a focus on RNAi and its role in contributing to disease pathology and in suppressing cancer." @default.
- W2894310390 created "2018-10-05" @default.
- W2894310390 creator A5026455270 @default.
- W2894310390 creator A5026756753 @default.
- W2894310390 creator A5056606410 @default.
- W2894310390 creator A5091274292 @default.
- W2894310390 date "2018-10-01" @default.
- W2894310390 modified "2023-10-03" @default.
- W2894310390 title "Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer" @default.
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