Abstract 4901: Impact of the TGF-β1 isoform on p53 signalling in ovarian cancer cell lines in response to cisplatin
Bibliographic record
Abstract
Abstract Transforming growth factor β is a pleiotropic cytokine which inhibits cell growth, induces cellular differentiation, and can lead to cellular apoptosis under certain conditions. TGF-β is also involved in epithelial-mesenchymal transition (EMT), a phenomenon by which cells acquire a dedifferentiated phenotype and gain motility and invasive properties. In the present study, we investigated the impact of TGF-β1 on p53 mediated cellular signalling in ovarian cancer cell lines in response to cisplatin. Four cell lines with different p53 status: A2780 (wild-type p53), A2780CP (derived from A2780, resistant to cisplatin, one p53 allele mutated V172F and one p53 allele wild-type), OVCAR-3 (p53 mutated R248Q) and SKOV-3 (p53 negative) were used in the present study. Cells were co-treated with TGF-β1 (10ng/mL) and cisplatin (10μM) for 24 hours and protein levels were analysed by western blotting. Our results show that TGF-β1 inhibits cisplatin-induced apoptosis in SKOV-3 cells as demonstrated by reduced PARP cleavage and caspase-3 activation. However, the inhibition of cisplatin-induced apoptosis was not observed in cells with wild type or mutated p53. Co-treatment of TGF-β1 and cisplatin decreased the levels of phosphorylated/active Akt compared to cisplatin alone, suggesting that TGF-β1 promotes cisplatin-induced apoptosis in A2780 cells in part through p53. In addition, Mdm2 was cleaved in response to cisplatin treatment only in p53 wild-type expressing A2780 cells. The levels of the caspase inhibitor XIAP were also decreased in A2780 cells when treated with cisplatin. Together, these results suggest that TGF-β1 promotes apoptosis when used in combination with cisplatin in p53 wild-type ovarian cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4901. doi:1538-7445.AM2012-4901
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".