ArticleMolecular cancer2015
Upregulation of the inwardly rectifying potassium channel Kir2.1 (KCNJ2) modulates multidrug resistance of small-cell lung cancer under the regulation of miR-7 and the Ras/MAPK pathway.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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65 citing papers in PubMed, 99 citations in OpenAlex.
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
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- Phosphoinositide-dependent kinase 1 (PDK1) in cancer: molecular insights and therapeutic strategies.Frontiers in chemistry · 2026Review
- Targeting Ion Channels for Cancer Therapy: From Pathophysiological Mechanisms to Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- MiRNAs: main players of cancer drug resistance target ABC transporters.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Identification and functional characterization of glycosyltransferase-related biomarkers for tuberculosis diagnosis.AMB Express · 2025Article
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- KCNJ2 Facilitates Clear Cell Renal Cell Carcinoma Progression and Glucose Metabolism.International journal of genomics · 2025Article
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- The role and mechanism of IFITM1 in developing acquired cisplatin resistance in small cell lung cancer.Heliyon · 2024Article
- Novel RNA molecular bioengineering technology efficiently produces functional miRNA agents.RNA (New York, N.Y.) · 2024Article
- The Screening of microRNAs in Chronic Myeloid Leukemia: A Clinical Evaluation.International journal of molecular sciences · 2024Article
- Knockdown of circZMIZ1 enhances the anti-tumor activity of CD8Functional & integrative genomics · 2024Article
- Prognostic implications of metabolism-related genes in acute myeloid leukemia.Frontiers in genetics · 2024Article
- Expression ofFrontiers in oncology · 2024Article
- Hydroquinidine Demonstrates Remarkable Antineoplastic Effects on Non-small Cell Lung Cancer Cells.Current molecular medicine · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- KCNAB2 overexpression inhibits human non-small-cell lung cancer cell growth in vitro and in vivo.Cell death discovery · 2023Article
- The development of radioresistant oral squamous carcinoma cell lines and identification of radiotherapy-related biomarkers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
5 more citing papers are in PubMed but not listed here.
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7 authors at 4 institutions in 1 country.
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Abstract
backgroundKCNJ2/Kir2.1, a member of the classical inwardly rectifying potassium channel family, is commonly expressed in a wide range of tissues and cell types. Previous studies indicated that Kir2.1 may be associated with SCLC multidrug resistance (MDR). However, whether Kir2.1 can regulate MDR and its underlying mechanisms remain poorly understood in SCLC.
methodsKCNJ2/Kir2.1 expression was examined in tissues from fifty-two SCLC cases by immunohistochemistry. Overexpression or knockdown of KCNJ2/Kir21 was performed in multidrug-resistant SCLC cell lines (H69AR and H446AR) and their parental cell lines (H69 and H446) to assess its influence on cell growth, apoptosis, the cell cycle and chemoresistance.
resultsKCNJ2/Kir2.1 was expressed in 44.23% (23/52) of SCLC tissues. Overexpression of KCNJ2/Kir2.1 was correlated with the clinical stage and chemotherapy response in SCLC patients. Knockdown of KCNJ2/Kir2.1 expression using KCNJ2/Kir2.1 shRNA in H69AR and H446AR cells inhibited cell growth and sensitized the cancer cells to chemotherapeutic drugs by increasing cell apoptosis and cell cycle arrest. Forced KCNJ2/Kir2.1 expression in H69 and H446 cells promoted cell growth and enhanced multidrug resistance via reduced drug-induced apoptosis accompanied by cell cycle arrest. KCNJ2/Kir2.1 expression was also influenced by PKC and MEK inhibitors. In addition, multidrug resistance protein 1 (MRP1/ABCC1) was confirmed to interact with KCNJ2/Kir2.1 by Co-IP assays.
conclusionsKCNJ2/Kir2.1 modulates cell growth and drug resistance by regulating MRP1/ABCC1 expression and is simultaneously regulated by the Ras/MAPK pathway and miR-7. KCNJ2/Kir2.1 may be a prognostic predictor and a potentially novel target for interfering with chemoresistance in SCLC.
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