Short-hairpin RNA-mediated suppression of cortactin may inhibit the migration and invasion abilities of endometrial cancer cells by reducing lamellipodia.
Cell migration
Cortactin
Endometrial neoplasms
Pseudopodia
Rac1
Journal
Iranian journal of basic medical sciences
ISSN: 2008-3866
Titre abrégé: Iran J Basic Med Sci
Pays: Iran
ID NLM: 101517966
Informations de publication
Date de publication:
2023
2023
Historique:
received:
18
09
2022
accepted:
30
05
2023
medline:
16
11
2023
pubmed:
16
11
2023
entrez:
16
11
2023
Statut:
ppublish
Résumé
The prognosis of endometrial cancer (EC) is significantly affected by tumor infiltration and metastasis. Cortactin (CTTN) regulates infiltration and metastasis in other tumors. Studies on the role and mechanism of CTTN in EC are limited and further studies are needed. Quantitative PCR and immunohistochemistry were used to detect Ras-associated C3 botulinum toxin substrate 1 (Rac1) and CTTN in EC and normal tissues. The relationship between the expression of these two genes and their prognostic factors was analyzed. A CTTN-RNAi lentiviral system was constructed and transfected into EC cells. Migration and invasion were evaluated by scratch assay, transwell migration, and invasion assays. Pseudopodia formation was observed by immunofluorescence staining. Western blotting was performed to detect the expression of Rac1. The expression levels of Rac1 and CTTN in EC tissues were significantly higher than those in normal tissues. In the EC group, Rac1 and CTTN levels were correlated. The protein expression levels of Rac1 and CTTN were related to myometrial invasion and stage. After CTTN knockdown, the migration rate, invasiveness, and migratory ability of EC cells decreased significantly. Lamellipodia was observed to disappear with the appearance of blebs. Rac1 protein expression was decreased after CTTN knockdown. CTTN may promote the invasion and migration of EC by lamellipodia. This effect may be related to the regulation of Rac1 by CTTN.
Identifiants
pubmed: 37970440
doi: 10.22038/IJBMS.2023.67633.14863
pmc: PMC10634056
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1390-1399Déclaration de conflit d'intérêts
The authors have no conflicts of interest to declare.
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