ArticleCancer biology & therapy2013
Mitogen-activated protein kinase phosphatase-1 inhibition and sustained extracellular signal-regulated kinase 1/2 activation in camptothecin-induced human colon cancer cell death.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- MicroRNA-873 Suppresses Viability and Invasion of Colorectal Cancer Through KRAS/MAPK Signaling and Sensitizes Tumor Spheroids to 5-Fluorouracil in a 3D Microwell Model.IEEE open journal of engineering in medicine and biology · 2026Article
- Dual-Specificity Protein Phosphatases Targeting Extracellular Signal-Regulated Kinases: Friends or Foes in the Biology of Cancer?International journal of molecular sciences · 2025Review
- 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
- ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.Cells · 2021Review
- Transcriptome analysis of potential candidate genes and molecular pathways in colitis-associated colorectal cancer of Mkp-1-deficient mice.BMC cancer · 2021Article
- Correlation of ERK/MAPK signaling pathway with proliferation and apoptosis of colon cancer cells.Oncology letters · 2019Article
- MKP-4 suppresses hepatocarcinogenesis by targeting ERK1/2 pathway.Cancer cell international · 2019Article
- Camptothecin inhibits the progression of NPC by regulating TGF-β-induced activation of the PI3K/AKT signaling pathway.Oncology letters · 2018Article
- NSC 95397 Suppresses Proliferation and Induces Apoptosis in Colon Cancer Cells through MKP-1 and the ERK1/2 Pathway.International journal of molecular sciences · 2018Article
- Regulatory Roles of MAPK Phosphatases in Cancer.Immune network · 2016Review
- ERK mediated upregulation of death receptor 5 overcomes the lack of p53 functionality in the diaminothiazole DAT1 induced apoptosis in colon cancer models: efficiency of DAT1 in Ras-Raf mutated cells.Molecular cancer · 2016Article
- Dengue-induced autophagy, virus replication and protection from cell death require ER stress (PERK) pathway activation.Cell death & disease · 2016Article
- ERK plays the baddie (again).Cancer biology & therapy · 2013Article
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6 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Camptothecins are commonly used chemotherapeutics; in some models, they enhance signaling via the mitogen-activated protein kinase (MAPK) pathway through effects on upstream kinases. To evaluate the impact of camptothecin (CPT) on MAPKs in human colon cancer, we studied HCT116 and CaCo2 colon cancer cells. We found that HCT116 cells highly express mitogen-activated protein kinase phosphatase-1 (MKP1), which selectively inactivates extracellular signal-regulated kinase (ERK), whereas MKP1 levels were undetectable in CaCo2 cells. CPT did not affect ERK activity in CaCo2 cells, but did induce a striking increase in ERK activity in HCT116 cells in association with a corresponding decrease in MKP1. The reduction in MKP1 expression occurred at a posttranscriptional level and was blocked by the proteasome inhibitor MG132, whereas that CPT-induced downregulation of MKP1 was not due to proteasome-mediated degradation. Treatment of HCT116 cells with CPT induced a sustained activation of nuclear ERK, which was required for CPT-induced apoptosis. P38 and JNK activity were unaffected by CPT, suggesting that the effects of CPT are mediated specifically by ERK. These results suggest that targeting dual-specificity MAPK phosphatases in colon cancer cells may be a viable strategy for optimizing camptothecin-based therapeutic protocols.
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