ArticleOncology letters2014
Cisplatin resistance by induction of aldo-keto reductase family 1 member C2 in human bladder cancer cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Role of Aldo-Keto reductase family 1 member C in cancer progression: a special focus on the role of AKR1C1 in pancreatic cancer.Medical oncology (Northwood, London, England) · 2025Article
- The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation.Cancers · 2025Article
- AKR1C2 silencing promotes ferroptosis and inhibits proliferation, migration, and invasion in lung cancer cells.PloS one · 2025Article
- Characterization of circulating tumor cells in patients with metastatic bladder cancer utilizing functionalized microfluidics.Neoplasia (New York, N.Y.) · 2024Article
- Review
- Cisplatin-Resistant Urothelial Bladder Cancer Cells Undergo Metabolic Reprogramming beyond the Warburg Effect.Cancers · 2024Article
- The effect of the alpha-specific PI3K inhibitor alpelisib combined with anti-HER2 therapy in HER2+/PIK3CA mutant breast cancer.Frontiers in oncology · 2023Article
- EHF is a novel regulator of cellular redox metabolism and predicts patient prognosis in HNSCC.NAR cancer · 2022Article
- Aberrant expression of claudin-6 contributes to malignant potentials and drug resistance of cervical adenocarcinoma.Cancer science · 2022Article
- Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies.Molecules (Basel, Switzerland) · 2021Review
- Identification of novel activators of the metal responsive transcription factor (MTF-1) using a gene expression biomarker in a microarray compendium.Metallomics : integrated biometal science · 2020Article
- AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway.Journal of cellular and molecular medicine · 2020Article
- Article
- Cisplatin-Based Chemotherapy of Human Cancers.Journal of cancer science & therapy · 2019Article
- Latent Kaposi's sarcoma-associated herpesvirus infection in bladder cancer cells promotes drug resistance by reducing reactive oxygen species.Journal of microbiology (Seoul, Korea) · 2016Article
- Aldo-keto reductase 1C1 induced by interleukin-1β mediates the invasive potential and drug resistance of metastatic bladder cancer cells.Scientific reports · 2016Article
- Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells.Oncology letters · 2016Article
- Article
- A Mechanism for the Temporal Potentiation of Genipin to the Cytotoxicity of Cisplatin in Colon Cancer Cells.International journal of medical sciences · 2016Article
- Inhibition of beclin1 affects the chemotherapeutic sensitivity of osteosarcoma.International journal of clinical and experimental pathology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is currently the most effective anti-tumor agent available against bladder cancer. To clarify the mechanism underlying cisplatin resistance in bladder cancer, the present study examined the role of the aldo-keto reductase family 1 member C2 (AKR1C2) protein on chemoresistance using a human bladder cancer cell line. The function of AKR1C2 in chemoresistance was studied using the human HT1376 bladder cancer cell line and the cisplatin-resistant HT1376-CisR subline. AKR1C2 was expressed in HT1376-CisR cells, but not in the parental cells. The effect of small interfering (si) RNAs and an inhibitor targeting AKR1C2 was examined to determine whether cisplatin sensitivity can be rescued by blocking AKR1C2 expression or function. Silencing of AKR1C2 mRNA or inhibition of AKR1C2 by 5β-cholanic acid resulted in a decrease in the survival of cells following cisplatin exposure. Intracellular accumulation of reactive oxygen species (ROS) was determined using a 2,7-dichlorodihydrofluorescein diacetate (H
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