ArticleInternational journal of molecular sciences2021
Transcriptomic Profiling Reveals AKR1C1 and AKR1C3 Mediate Cisplatin Resistance in Signet Ring Cell Gastric Carcinoma via Autophagic Cell Death.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Silencing of SIVA‑1 promotes cisplatin resistance in gastric cancer via the Bcl‑2/BAX‑mediated mitochondria‑dependent apoptosis pathway.Oncology reports · 2026Article
- Targeting AKR1C1 overcomes lenvatinib resistance in hepatocellular carcinoma through the STAT3-ABC transporters pathway.Journal of gastrointestinal oncology · 2026Article
- Natural simple coumarins and their interaction with AKR1C3: implications for overcoming chemoradioresistance in gastrointestinal carcinomas.Medical oncology (Northwood, London, England) · 2026Article
- A comprehensive proteomic analysis uncovers novel molecular subtypes of gastric signet ring cell carcinoma: Identification of potential prognostic biomarkers and therapeutic targets.Genes & diseases · 2026Article
- 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
- Mapping the landscape of gastric signet ring cell carcinoma: Overcoming hurdles and charting new paths for advancement.World journal of clinical oncology · 2025Article
- AKR1C1 interacts with STAT3 to increase intracellular glutathione and confers resistance to oxaliplatin in colorectal cancer.Acta pharmaceutica Sinica. B · 2024Article
- AKR1C3 promotes progression and mediates therapeutic resistance by inducing epithelial-mesenchymal transition and angiogenesis in small cell lung cancer.Translational oncology · 2024Article
- Defining the biological functions and clinical significance of AKR1C3 in gastric carcinogenesis through multiomics functional analysis and immune infiltration analysis.Journal of Cancer · 2024Article
- AKR1C3 in carcinomas: from multifaceted roles to therapeutic strategies.Frontiers in pharmacology · 2024Review
- Prognostic Survival Significance of Signet Ring Cell (SRC) Gastric Cancer: Retrospective Analysis from a Single Western Center.Journal of personalized medicine · 2023Article
- Diclofenac Sensitizes Signet Ring Cell Gastric Carcinoma Cells to Cisplatin by Activating Autophagy and Inhibition of Survival Signal Pathways.International journal of molecular sciences · 2022Article
- An Oleocanthal-Enriched EVO Oil Extract Induces the ROS Production in Gastric Cancer Cells and Potentiates the Effect of Chemotherapy.Antioxidants (Basel, Switzerland) · 2022Article
- PredictiveNetwork: predictive gene network estimation with application to gastric cancer drug response-predictive network analysis.BMC bioinformatics · 2022Article
- Is Autophagy Always a Barrier to Cisplatin Therapy?Biomolecules · 2022Review
- Wogonin increases gemcitabine sensitivity in pancreatic cancer by inhibiting Akt pathway.Frontiers in pharmacology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Signet ring cell gastric carcinoma (SRCGC) is a lethal malignancy that has developed drug resistance to cisplatin therapies. The aim of this study was to characterize the acquisition of the cisplatin-resistance SRCGC cell line (KATO/DDP cells) and to understand the molecular mechanisms underlying cisplatin resistance. Transcriptomic and bioinformatic analyses were used to identify the candidate gene. This was confirmed by qPCR and Western blot. Aldoketoreductase1C1 and 1C3 (AKR1C1 and AKR1C3) were the most promising molecules in KATO/DDP cells. A specific inhibitor of AKR1C1 (5PBSA) and AKR1C3 (ASP9521) was used to enhance cisplatin-induced KATO/DPP cell death. Although cisplatin alone induced KATO/DDP apoptosis, a combination treatment of cisplatin and the AKR1C inhibitors had no influence on percent cell apoptosis. In conjunction with the autophagy inhibitor, 3MA, attenuated the effects of 5PBSA or ASP9521 to enhance cisplatin-induced cell death. These results indicated that AKR1C1 and 1C3 regulated cisplatin-induced KATO/DDP cell death via autophagy. Moreover, cisplatin in combination with AKR1C inhibitors and N-acetyl cysteine increased KATO/DDP cells' viability when compared with a combination treatment of cisplatin and the inhibitors. Taken together, our results suggested that AKR1C1 and 1C3 play a crucial role in cisplatin resistance of SRCGC by regulating redox-dependent autophagy.
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