Complex roles of the actin-binding protein Girdin/GIV in DNA damage-induced apoptosis of cancer cells.
Aged
Aged, 80 and over
Animals
Apoptosis
/ genetics
Biomarkers
Cell Cycle
Cell Line, Tumor
DNA Damage
/ radiation effects
Esophageal Neoplasms
/ genetics
Female
HeLa Cells
Humans
Male
Microfilament Proteins
/ genetics
Middle Aged
Mitosis
Models, Biological
Neoplasm Grading
Neoplasm Staging
Neoplasms
/ genetics
Prognosis
Ultraviolet Rays
Vesicular Transport Proteins
/ genetics
DNA damage
Girdin
apoptosis
cancer cell heterogeneity
cell cycle
cell migration
Journal
Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
11
05
2020
revised:
19
08
2020
accepted:
23
08
2020
pubmed:
3
9
2020
medline:
22
12
2020
entrez:
3
9
2020
Statut:
ppublish
Résumé
The actin-binding protein Girdin is a hub protein that interacts with multiple proteins to regulate motility and Akt and trimeric G protein signaling in cancer cells. Girdin expression correlates with poor outcomes in multiple human cancers. However, those findings are not universal, as they depend on study conditions. Those data suggest that multiple aspects of Girdin function and its role in tumor cell responses to anticancer therapeutics must be reconsidered. In the present study, we found that Girdin is involved in DNA damage-induced cancer cell apoptosis. An esophageal cancer cell line that exhibited high Girdin expression showed a marked sensitivity to UV-mediated DNA damage compared to a line with low Girdin expression. When transcriptional activation of endogenous Girdin was mediated by an engineered CRISPR/Cas9 activation system, sensitivity to DNA damage increased in both stationary and migrating HeLa cancer cells. High Girdin expression was associated with dysregulated cell cycle progression and prolonged G
Identifiants
pubmed: 32875699
doi: 10.1111/cas.14637
pmc: PMC7648047
doi:
Substances chimiques
Biomarkers
0
CCDC88A protein, human
0
Microfilament Proteins
0
Vesicular Transport Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
4303-4317Subventions
Organisme : Japan Agency for Medical Research and Development
ID : 19cm0106332h0002
Organisme : Japan Agency for Medical Research and Development
ID : 19gm0810007h0104
Organisme : Japan Agency for Medical Research and Development
ID : 19gm1210008s0101
Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan
ID : 18H02638
Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan
ID : 26221304
Informations de copyright
© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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