ArticleGynecologic oncology2012
The BCL2 antagonist of cell death pathway influences endometrial cancer cell sensitivity to cisplatin.
Article in Gynecologic oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The sulfonamide anticancer agent indisulam enhances the chemosensitivity of gastric cancer cells by targeting FKBP8.The FEBS journal · 2026Article
- Inhibition of BAD-Ser99 phosphorylation synergizes with PARP inhibition to ablate PTEN-deficient endometrial carcinoma.Cell death & disease · 2022Article
- Emerging role of BAD and DAD1 as potential targets and biomarkers in cancer.Oncology letters · 2021Review
- Systematic analysis of ovarian cancer platinum-resistance mechanisms via text mining.Journal of ovarian research · 2020Article
- Expression of the BAD pathway is a marker of triple-negative status and poor outcome.Scientific reports · 2019Article
- Long Non-coding RNA CDKN2B Antisense RNA 1 Gene Contributes to Paclitaxel Resistance in Endometrial Carcinoma.Frontiers in oncology · 2019Article
- Combined Inhibition of Both p110α and p110β Isoforms of Phosphatidylinositol 3-Kinase Is Required for Sustained Therapeutic Effect in PTEN-Deficient, ERClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Growth Hormone differentially modulates chemoresistance in human endometrial adenocarcinoma cell lines.Endocrine · 2017Article
- Depletion of UBA protein 2-like protein inhibits growth and induces apoptosis of human colorectal carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Molecular determinants for lymph node metastasis in clinically early-stage endometrial cancer.Oncology letters · 2016Article
- BAD-mediated apoptotic pathway is associated with human cancer development.International journal of molecular medicine · 2015Article
- Preparation and characterization of cisplatin magnetic solid lipid nanoparticles (MSLNs): effects of loading procedures of Fe3O4 nanoparticles.Pharmaceutical research · 2015Article
- Systems biology of cisplatin resistance: past, present and future.Cell death & disease · 2014Review
- Androgen receptor increases CD133 expression and progenitor-like population that associate with cisplatin resistance in endometrial cancer cell line.Reproductive sciences (Thousand Oaks, Calif.) · 2014Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo identify pathways that influence endometrial cancer (EC) cell sensitivity to cisplatin and to characterize the BCL2 antagonist of cell death (BAD) pathway as a therapeutic target to increase cisplatin sensitivity.
methodsEight EC cell lines (Ishikawa, MFE296, RL 95-2, AN3CA, KLE, MFE280, MFE319, HEC-1-A) were subjected to Affymetrix Human U133A GeneChip expression analysis of approximately 22,000 probe sets. In parallel, endometrial cell line sensitivity to cisplatin was quantified by MTS assay, and IC(50) values were calculated. Pearson's correlation test was used to identify genes associated with response to cisplatin. Genes associated with cisplatin responsiveness were subjected to pathway analysis. The BAD pathway was identified and subjected to targeted modulation, and the effect on cisplatin sensitivity was evaluated.
resultsPearson's correlation analysis identified 1443 genes associated with cisplatin resistance (P<0.05), which included representation of the BAD-apoptosis pathway. Small interfering RNA (siRNA) knockdown of BAD pathway protein phosphatase PP2C expression was associated with increased phosphorylated BAD (serine-155) levels and a parallel increase in cisplatin resistance in Ishikawa (P=0.004) and HEC-1-A (P=0.02) cell lines. In contrast, siRNA knockdown of protein kinase A expression increased cisplatin sensitivity in the Ishikawa (P=0.02) cell line.
conclusionThe BAD pathway influences EC cell sensitivity to cisplatin, likely via modulation of the phosphorylation status of the BAD protein. The BAD pathway represents an appealing therapeutic target to increase EC cell sensitivity to cisplatin.
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