ArticleJournal of cellular physiology2019
The atypical MAPK ERK3 potently suppresses melanoma cell growth and invasiveness.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 18 citations in OpenAlex.
- Long non-coding RNA IL6-AS1 promotes severe community-acquired pneumonia in children through the miR-149-5p/MAPK6 axis.BMC pediatrics · 2026Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- ERK3 is involved in regulating cardiac fibroblast function.Physiological reports · 2024Article
- Review
- Article
- Proteomic analysis of holocarboxylase synthetase deficient-MDA-MB-231 breast cancer cells revealed the biochemical changes associated with cell death, impaired growth signaling, and metabolism.Frontiers in molecular biosciences · 2023Article
- Conditional ERK3 overexpression cooperates with PTEN deletion to promote lung adenocarcinoma formation in mice.Molecular oncology · 2022Article
- FBXW7-mediated ERK3 degradation regulates the proliferation of lung cancer cells.Experimental & molecular medicine · 2022Article
- Integrated Analysis of DNA methylation and transcriptome profile to identify key features of age-related macular degeneration.Bioengineered · 2021Article
- MAPK6-AKT signaling promotes tumor growth and resistance to mTOR kinase blockade.Science advances · 2021Article
- ERK3 is transcriptionally upregulated by ∆Np63α and mediates the role of ∆Np63α in suppressing cell migration in non-melanoma skin cancers.BMC cancer · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitogen-activated protein kinase 6 (MAPK6) represents an atypical MAPK also known as extracellular signal-regulated kinase 3 (ERK3), which has been shown to play roles in cell motility and metastasis. ERK3 promotes migration and invasion of lung cancer cells and head and neck cancer cells by regulating the expression and/or activity of proteins involved in cancer progression. For instance, ERK3 upregulates matrix metallopeptidases and thereby promotes cancer cell invasiveness, and it phosphorylates tyrosyl-DNA phosphodiesterase 2, thereby enhancing chemoresistance in lung cancer. Here we discovered that ERK3 plays a converse role in melanoma. We observed that BRAF, an oncogenic Ser/Thr kinase, upregulates ERK3 expression levels by increasing both ERK3 messenger RNA levels and protein stability. Interestingly, although BRAF's kinase activity was required for upregulating ERK3 gene transcription, BRAF stabilized ERK3 protein in a kinase-independent fashion. We further demonstrate that ERK3 inhibits the migration, proliferation and colony formation of melanoma cells. In line with this, high level of ERK3 predicted increased survival among patients with melanomas. Taken together, these results indicate that ERK3 acts as a potent suppressor of melanoma cell growth and invasiveness.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.