ArticleOncology letters2013
Overexpression of MEKK2 is associated with colorectal carcinogenesis.
Article in Oncology letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Structural basis for MEKK2 dimerization and substrate recognition.Nature communications · 2025Article
- Review
- MAP3K2 augments Th1 cell differentiation via IL-18 to promote T cell-mediated colitis.Science China. Life sciences · 2021Article
- MEKK2 and MEKK3 suppress Hedgehog pathway-dependent medulloblastoma by inhibiting GLI1 function.Oncogene · 2018Article
- Discovery and characterization of an iminocoumarin scaffold as an inhibitor of MEKK2 (MAP3K2).Biochemical and biophysical research communications · 2018Article
- Oncogenic signaling of MEK5-ERK5.Cancer letters · 2017Review
- Identification of ponatinib and other known kinase inhibitors with potent MEKK2 inhibitory activity.Biochemical and biophysical research communications · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein kinase kinase kinase 2 (MEKK2) is an important upstream mediator of the extracellular signal-regulated kinase 5 signaling cascade that is essential for a number of cellular functions, including mitogenesis, differentiation and oncogenic transformation. Using western blotting to examine MEKK2 expression in 16 cases of primary colorectal cancer (CRC) lesions with paired normal mucosa, it was identified that MEKK2 is highly expressed in CRC lesions compared with that of the normal mucosa. Immunohistochemistry of 24 normal mucosa, 24 adenoma and 96 adenocarcinoma colorectal specimens indicated that the expression of MEKK2 was significantly increased in the adenoma and carcinoma specimens compared with that of the normal mucosa cases (P<0.0001 for both). However, no significant differences were detected in MEKK2 expression between the carcinoma and adenoma specimens (P=0.85). Similarly, no correlations were identified between MEKK2 expression and clinicopathological features, including gender, age, body mass index, histological differentiation, depth of invasion, lymph node metastasis, UICC stage and K-ras mutations (P>0.05). The present study demonstrated that MEKK2 functions as a promotive factor in CRC.
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Registered trials
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