ArticleJournal of biochemical and molecular toxicology2023
Gemcitabine resistance in non-small cell lung cancer is mediated through activation of the PI3K/AKT/NF-κB pathway and suppression of ERK signaling by reactive oxygen species.
Article in Journal of biochemical and molecular toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The Managed Acquisition of Chemoresistance as an Informative Tool for Tumor Research.International journal of molecular sciences · 2025Review
- Network pharmacology and experimental analysis reveal Ethyl caffeate delays osimertinib resistance in lung cancer by suppression of MET.Cancer cell international · 2025Article
- Single-cell and Multi-omics Analysis Confirmed the Signature and Potential Targets of Cuproptosis in Colorectal Cancer.Journal of Cancer · 2025Article
- KRAS G12C inhibition enhances efficacy to conventional chemotherapy in KRAS-mutant NSCLC.Frontiers in oncology · 2025Article
- Pharmacology, medical uses, and clinical translational challenges of Saikosaponin A: A review.Heliyon · 2024Review
- Establishment and characterization of the gemcitabine-resistant human gallbladder cancer cell line NOZ GemR.Annals of medicine and surgery (2012) · 2024Article
- The novel miR-873-5p-YWHAE-PI3K/AKT axis is involved in non-small cell lung cancer progression and chemoresistance by mediating autophagy.Functional & integrative genomics · 2024Article
- Gemcitabine resistance in non-small cell lung cancer is mediated through activation of the PI3K/AKT/NF-κB pathway and suppression of ERK signaling by reactive oxygen species.Journal of biochemical and molecular toxicology · 2023Article
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Authors and funding
11 authors.
Funding
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Abstract
Lung cancer is one of the most common cancers in the world. Chemotherapy is a standard clinical treatment. However, tumor cells often develop multidrug resistance after chemotherapy, an inevitable bottleneck in cancer treatment. Therefore, this study used gemcitabine-resistant (GEM-R) CL1-0 lung cancer cells. First, we used flow cytometry and western blot analysis to examine differences in performance between resistant and parental cells. The results showed that compared with parental cells, GEM-R CL1-0 cells significantly enhanced the activation of the AKT pathway, which promoted survival and growth, and decreased the activation of the reactive oxygen species-extracellular signal-regulated kinase (ROS)-ERK pathway. Next, the AKT and ERK pathways' role in tumor growth was further explored in vivo using a xenograft model. The results showed that enhancing AKT and inhibiting ERK activation reduced GEM-induced inhibition of tumor growth. Finally, combining the above results, we found that GEM-R CL1-0 cells showed reduced sensitivity to GEM by activating the phosphatidylinositol 3-kinase/AKT/NF-kB pathway and inhibiting the ROS-ERK pathway leading to resistance against GEM. Therefore, the AKT and ERK pathways are potential targets for improving the sensitivity of cancer cells to anticancer drugs.
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