ArticleOncotarget2016
Mitomycin C treatment induces resistance and enhanced migration via phosphorylated Akt in aggressive lung cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 7 citations in OpenAlex.
- β-Thujaplicin modulates the ODC-ROS-linked apoptosis in H460 lung cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- New Dihalogenated Derivatives of Condensed Benzimidazole Diones Promotes Cancer Cell Death Through Regulating STAT3/HK2 Axis/Pathway.Molecules (Basel, Switzerland) · 2025Article
- Combining Mitomycin C with inhibition of BAD phosphorylation enhances apoptotic cell death in advanced cervical cancer.Translational oncology · 2024Article
- Electrochemotherapy with Mitomycin C Potentiates Apoptosis Death by Inhibiting Autophagy in Squamous Carcinoma Cells.Cancers · 2021Article
- Perspectives and controversies regarding the use of natural products for the treatment of lung cancer.Cancer medicine · 2021Review
- Article
- Concise Polygenic Models for Cancer-Specific Identification of Drug-Sensitive Tumors from Their Multi-Omics Profiles.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since 1984, mitomycin C (MMC) has been applied in the treatment of non-small-cell lung cancer (NSCLC). MMC-based chemotherapeutic regimens are still under consideration owing to the efficacy and low cost as compared with other second-line regimens in patients with advanced NSCLC. Hence, it is important to investigate whether MMC induces potential negative effects in NSCLC. Here, we found that the malignant lung cancer cells, CL1-2 and CL1-5, were more resistant to MMC than were the parental CL1-0 cells and pre-malignant CL1-1 cells. CL1-2 and CL1-5 cells consistently showed lower sub-G1 fractions post MMC treatment. DNA repair-related proteins were not induced more in CL1-5 than in CL1-0 cells, but the levels of endogenous and MMC-induced phosphorylated Akt (p-Akt) were higher in CL1-5 cells. Administering a p-Akt inhibitor reduced the MMC resistance, demonstrating that p-Akt is important in the MMC resistance of CL1-5 cells. Furthermore, we revealed that cell migration was enhanced by MMC but lowered by a p-Akt inhibitor in CL1-5 cells. This study suggests that in CL1-5 cells, the activity of p-Akt, rather than DNA repair mechanisms, may underlie the resistance to MMC and enhance the cells' migration abilities after MMC treatment.
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