Downregulation of TGF-ß1 suppressed proliferation and increased chemosensitivity of ovarian cancer cells by promoting BRCA1/Smad3 signaling
Biol. Res
; 51: 58, 2018. graf
Article
in En
| LILACS
| ID: biblio-1011402
Responsible library:
CL1.1
ABSTRACT
BACKGROUND:
Studies have demonstrated that transforming growth factor beta-1 (TGF-ß1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC). However, its regulatory mechanism in OC and whether TGF-ß1 is involved in chemosensitivity regulation remains unclear. Thus, the aim of this study was to investigate the role of TGF-ß1 in OC.METHODS:
The OC cell line SKOV3 was employed, and TGF-ß1 overexpression or knockdown vectors were constructed. The cell proliferation of SKOV3 was evaluated with the cell counting kit (CCK8) kit after treatment with different concentrations of cis-platinum. Western blot and protein immunoprecipitation were employed to detect changes in BRCA1 and Smad3 expression and their interactions. Tumor growth in nude mice was evaluated.RESULTS:
The results showed that TGF-ß1 knockdown increased chemosensitivity by promoting BRCA1 expression and Smad3 phosphorylation. In vivo studies showed that TGF-ß1 knockdown significantly inhibited the growth of tumors, also by upregulating BRCA1 expression and Smad3 phosphorylation.CONCLUSION:
Taken together, our results suggest that TGF-ß1 knockdown inhibits tumor growth and increases chemosensitivity by promotion of BRCA1/Smad3 signaling.Key words
Full text:
1
Index:
LILACS
Main subject:
Ovarian Neoplasms
/
Down-Regulation
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Genes, BRCA1
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Smad3 Protein
/
Transforming Growth Factor beta1
Limits:
Animals
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Female
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Humans
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Male
Language:
En
Journal:
Biol. Res
Journal subject:
BIOLOGIA
Year:
2018
Type:
Article