Mitochondrial Fus1/Tusc2 and cellular Ca2


Journal

Cancer gene therapy
ISSN: 1476-5500
Titre abrégé: Cancer Gene Ther
Pays: England
ID NLM: 9432230

Informations de publication

Date de publication:
10 2022
Historique:
received: 13 10 2021
accepted: 28 01 2022
revised: 22 12 2021
pubmed: 20 2 2022
medline: 20 10 2022
entrez: 19 2 2022
Statut: ppublish

Résumé

FUS1/TUSC2 (FUSion1/TUmor Suppressor Candidate 2) is a tumor suppressor gene (TSG) originally described as a member of the TSG cluster from human 3p21.3 chromosomal region frequently deleted in lung cancer. Its role as a TSG in lung, breast, bone, and other cancers was demonstrated by several groups, but molecular mechanisms of its activities are starting to unveil lately. They suggest that Fus1-dependent mechanisms are relevant in etiologies of diseases beyond cancer, such as chronic inflammation, bacterial and viral infections, premature aging, and geriatric diseases. Here, we revisit the discovery of FUS1 gene in the context of tumor initiation and progression, and review 20 years of research into FUS1 functions and its molecular, structural, and biological aspects that have led to its use in clinical trials and gene therapy. We present a data-driven view on how interactions of Fus1 with the mitochondrial Ca

Identifiants

pubmed: 35181743
doi: 10.1038/s41417-022-00434-9
pii: 10.1038/s41417-022-00434-9
pmc: PMC9576590
doi:

Substances chimiques

Anti-Inflammatory Agents 0
Tumor Suppressor Proteins 0
TUSC2 protein, human 0

Types de publication

Journal Article Review Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1307-1320

Subventions

Organisme : NCI NIH HHS
ID : SC1 CA182843
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA163069
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007593
Pays : United States

Informations de copyright

© 2022. The Author(s).

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Auteurs

Roman Uzhachenko (R)

Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.

Akiko Shimamoto (A)

Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.
Vanderbilt Memory and Alzheimer's Center, Vanderbilt University, Nashville, TN, USA.

Sanika S Chirwa (SS)

Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.

Sergey V Ivanov (SV)

Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.

Alla V Ivanova (AV)

School of Graduate Studies and Research, Meharry Medical College, Nashville, TN, USA. aivanova@mmc.edu.

Anil Shanker (A)

Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA. ashanker@mmc.edu.
Host-Tumor Interactions Research Program, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA. ashanker@mmc.edu.
Vanderbilt Institute for Infection, Immunology and Inflammation, Vanderbilt University, Nashville, TN, USA. ashanker@mmc.edu.
Vanderbilt Memory and Alzheimer's Center, Vanderbilt University, Nashville, TN, USA. ashanker@mmc.edu.

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