Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer

Andrea E. Murmann; Jindan Yu; Puneet Opal; Marcus E. Peter

doi:10.1016/j.trecan.2018.08.004

Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer

Andrea E. Murmann, Jindan Yu, Puneet Opal, Marcus E. Peter^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

18 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	684-700
Number of pages	17
Journal	Trends in Cancer
Volume	4
Issue number	10
DOIs	https://doi.org/10.1016/j.trecan.2018.08.004
State	Published - Oct 2018

Keywords

AR
Huntington's disease
RNA
SBMA
TNR
cancer

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.trecan.2018.08.004

Cite this

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title = "Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer",

abstract = "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.",

keywords = "AR, Huntington's disease, RNA, SBMA, TNR, cancer",

author = "Murmann, {Andrea E.} and Jindan Yu and Puneet Opal and Peter, {Marcus E.}",

note = "Funding Information: This work was funded by NIH grants R35CA197450 to M.E.P. and R01NS06251 to P.O. Publisher Copyright: {\textcopyright} 2018 Elsevier Inc.",

year = "2018",

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doi = "10.1016/j.trecan.2018.08.004",

language = "English (US)",

volume = "4",

pages = "684--700",

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AU - Murmann, Andrea E.

AU - Yu, Jindan

AU - Opal, Puneet

AU - Peter, Marcus E.

PY - 2018/10

Y1 - 2018/10

N2 - 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.

AB - 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.

KW - AR

KW - Huntington's disease

KW - RNA

KW - SBMA

KW - TNR

KW - cancer

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DO - 10.1016/j.trecan.2018.08.004

M3 - Review article

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JO - Trends in Cancer

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Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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