Expression, Interaction, and Role of Pseudogene Adh6-ps1 in Cancer and other Disease Phenotypes

Pseudogenes have been classified as functionless and their annotation is an ongoing problem. The Adh6-ps1—a mouse pseudogene belonging to the alcohol dehydrogenase gene complex (Adh) was analyzed to review the conservation, homology, expression and interactions, and identify any role it plays in dis...

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Bibliographic Details
Main Author: Martin C Nwadiugwu
Format: Article
Language:English
Published: SAGE Publishing 2021-08-01
Series:Bioinformatics and Biology Insights
Online Access:https://doi.org/10.1177/11779322211040591
Description
Summary:Pseudogenes have been classified as functionless and their annotation is an ongoing problem. The Adh6-ps1—a mouse pseudogene belonging to the alcohol dehydrogenase gene complex (Adh) was analyzed to review the conservation, homology, expression and interactions, and identify any role it plays in disease phenotypes using bioinformatics databases. Results showed that Adh6-ps1 have 2 transcripts (processed and unprocessed) which may have emerged from a transposition and duplication event, respectively, and that induced inversions (Uox gene, In(3)11Rk) involving gene complexes associated with Adh6-ps1 have been implicated in a diverse range of diseases. Adh6-ps1 is highly conserved in vertebrates particularly rodents, and expressed in the liver. The top 5 MirRNA targets identified are Mir455, Mir511, Mir1903, Mir361, and Mir669o markers. While much is unknown about Mir1903 and Mir669o, the silencing of Mir455 and Mir511 is linked with hepatocellular carcinoma (HCC), and Mir361 is implicated in endometrial cancers. Given the identified MirRNA interactions with Adh6-ps1 and their expression in cancer phenotypes, and Adh6-ps1 associations with induced inversions, it may well have a role in tumorigenesis and disease phenotypes. Nonetheless, further studies are required to establish these facts to add to the growing efforts to understand pseudogenes and their potential involvement in disease conditions.
ISSN:1177-9322