Abstract
Here we apply state-of-the-art CRISPR technologies to study the impact that PTENP1 pseudogene transcript has on the expression levels of its parental gene PTEN, and hence on the output of AKT signaling in cancer. Our data expand the repertoire of approaches that can be used to dissect competing endogenous RNA (ceRNA)-based interactions, while providing further experimental evidence in support of the very first one that we discovered.
Keywords:
CRISPR; Cas9-mediated knock-in; CasRx-mediated knock-down; PTEN; PTENP1; ceRNA.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / pathology
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Binding, Competitive
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CRISPR-Cas Systems*
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Cell Division
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Cell Line, Tumor
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Gene Expression Regulation, Neoplastic*
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Gene Knockdown Techniques
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Humans
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Male
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MicroRNAs / genetics
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MicroRNAs / metabolism
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics*
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PTEN Phosphohydrolase / biosynthesis
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PTEN Phosphohydrolase / genetics*
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Prostatic Neoplasms / pathology
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Proto-Oncogene Proteins c-akt / biosynthesis
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Proto-Oncogene Proteins c-akt / genetics
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Pseudogenes / genetics*
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RNA Interference
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RNA, Guide, CRISPR-Cas Systems / genetics
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
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RNA, Neoplasm / genetics*
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RNA, Neoplasm / metabolism
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RNA, Small Interfering / genetics
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RNA, Small Interfering / pharmacology
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Sequence Homology, Nucleic Acid
Substances
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MicroRNAs
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Neoplasm Proteins
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RNA, Guide, CRISPR-Cas Systems
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RNA, Messenger
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RNA, Neoplasm
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RNA, Small Interfering
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Proto-Oncogene Proteins c-akt
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PTEN Phosphohydrolase
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PTEN protein, human