ArticleThe American journal of pathology2009
Down-regulation of DUSP6 expression in lung cancer: its mechanism and potential role in carcinogenesis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 106 citations in OpenAlex.
- Dual-specificity phosphatase 6 interferes with the repressive activity of forkhead box O1 towards CYP4A11 that mediates lipid accumulation in the liver.Scientific reports · 2026Article
- Long non-coding RNAs and signaling networks in non-small cell lung cancer: mechanistic insights into tumor pathogenesis.Cancer gene therapy · 2025Review
- Scoparone attenuates PD-L1 expression in human breast cancer cells by MKP-3 upregulation.Animal cells and systems · 2024Article
- MAPK-negative feedback regulation confers dependence to JAK2Leukemia · 2023Article
- TFEB inhibition induces melanoma shut-down by blocking the cell cycle and rewiring metabolism.Cell death & disease · 2023Article
- Redifferentiated cardiomyocytes retain residual dedifferentiation signatures and are protected against ischemic injury.Nature cardiovascular research · 2023Article
- Suppression of mutant Kirsten-RAS (KRASOncogene · 2022Article
- Article
- Knockdown of TRIM9 attenuates irinotecan‑induced intestinal mucositis in IEC‑6 cells by regulating DUSP6 expression via the P38 pathway.Molecular medicine reports · 2021Article
- Loss of FBXO31-mediated degradation of DUSP6 dysregulates ERK and PI3K-AKT signaling and promotes prostate tumorigenesis.Cell reports · 2021Article
- The nonsmokers' and smokers' pathways in lung adenocarcinoma: Histological progression and molecular bases.Cancer science · 2021Review
- Tripartite motif protein 11 (TRIM11), an oncogene for human lung cancer via the DUSP6-mediated ERK1/2 signaling pathway.Cancer biology & therapy · 2021Article
- PPP6C negatively regulates oncogenic ERK signaling through dephosphorylation of MEK.Cell reports · 2021Article
- A Crosstalk Between Dual-Specific Phosphatases and Dual-Specific Protein Kinases Can Be A Potential Therapeutic Target for Anti-cancer Therapy.Advances in experimental medicine and biology · 2021Article
- ZNF251 promotes the progression of lung cancer by activating ERK signaling.Cancer science · 2020Article
- Overexpression of DUSP6 enhances chemotherapy-resistance of ovarian epithelial cancer by regulating the ERK signaling pathway.Journal of Cancer · 2020Article
- Knockdown of TRIM37 Promotes Apoptosis and Suppresses Tumor Growth in Gastric Cancer by Inactivation of the ERK1/2 Pathway.OncoTargets and therapy · 2020Article
- Targeted Inhibition of the Dual Specificity Phosphatases DUSP1 and DUSP6 Suppress MPNST Growth via JNK.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Regulation of Dual-Specificity Phosphatase (DUSP) Ubiquitination and Protein Stability.International journal of molecular sciences · 2019Review
- Inhibition of DUSP6 sensitizes ovarian cancer cells to chemotherapeutic agents via regulation of ERK signaling response genes.Oncotarget · 2019Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our preliminary studies revealed that oncogenic KRAS (KRAS/V12) dramatically suppressed the growth of immortalized airway epithelial cells (NHBE-T, with viral antigen-inactivated p53 and RB proteins). This process appeared to be a novel event, different from the so-called premature senescence that is induced by either p53 or RB, suggesting the existence of a novel tumor suppressor that functions downstream of oncogenic KRAS. After a comprehensive search for genes whose expression levels were modulated by KRAS/V12, we focused on DUSP6, a pivotal negative feedback regulator of the RAS-ERK pathway. A dominant-negative DUSP6 mutant, however, failed to rescue KRAS/V12-induced growth suppression, but conferred a stronger anchorage-independent growth activity to the surviving subpopulation of cells generated from KRAS/V12-transduced NHBE-T. DUSP6 expression levels were found to be weaker in most lung cancer cell lines than in NHBE-T, and DUSP6 restoration suppressed cellular growth. In primary lung cancers, DUSP6 expression levels decreased as both growth activity and histological grade of the tumor increased. Loss of heterozygosity of the DUSP6 locus was found in 17.7% of cases and was associated with reduced expression levels. These results suggest that DUSP6 is a growth suppressor whose inactivation could promote the progression of lung cancer. We have here identified an important factor involved in carcinogenesis through a comprehensive search for downstream targets of oncogenic KRAS.
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