ReviewCancers2016
MLK3 Signaling in Cancer Invasion.
Review in Cancers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
27 citing papers in PubMed, 53 citations in OpenAlex.
- Mechanism of RACK1-dependent ZAKα activation at stalled and collided ribosomes.Molecular cell · 2026Article
- Regulation of E-cadherin by mixed lineage kinase 3 (MLK3) mediates cell adhesion in ovarian cancer spheroids.Biochimica et biophysica acta. Molecular cell research · 2026Article
- Therapeutic limitations of oncolytic VSVd51-mediated miR-199a-5p delivery in triple negative breast cancer models.Scientific reports · 2025Article
- Mixed lineage kinase (MLK) controls tumor development and angiogenesis.Angiogenesis · 2025Article
- Key Mechanisms of Oxidative Stress-Induced Ferroptosis in Heart Failure with Preserved Ejection Fraction and Potential Therapeutic Approaches.Reviews in cardiovascular medicine · 2025Review
- MDNN-DTA: a multimodal deep neural network for drug-target affinity prediction.Frontiers in genetics · 2025Article
- The Expression Profiles and Clinical Significance of Mixed Lineage Kinases in Glioma.Mediators of inflammation · 2024Article
- TrkA expression directs the anti-neoplastic activity of MLK3 inhibitors in triple-negative breast cancer.Oncogene · 2023Article
- MLK3 silence suppressed osteogenic differentiation and delayed bone formation via influencing the bone metabolism and disturbing MAPK signaling.Journal of orthopaedic translation · 2023Article
- CRISPR/Cas9 as a therapeutic tool for triple negative breast cancer: from bench to clinics.Frontiers in molecular biosciences · 2023Review
- Bioinformatics and Experimental Analyses Reveal MAP4K4 as a Potential Marker for Gastric Cancer.Genes · 2022Article
- ZAK Gene Expression in Patients with Helicobacter pylori Infection.Journal of gastrointestinal cancer · 2022Article
- Mechanisms underlying melanoma invasion as a consequence of MLK3 loss.Experimental cell research · 2022Article
- Silence of MLK3 alleviates lipopolysaccharide-induced lung epithelial cell injury via inhibiting p53-mediated ferroptosis.Journal of molecular histology · 2022Article
- Metastasis and MAPK Pathways.International journal of molecular sciences · 2022Review
- MAP4K4 promotes pancreatic tumorigenesis via phosphorylation and activation of mixed lineage kinase 3.Oncogene · 2021Article
- Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer development.Cancer letters · 2021Article
- New Insights into the Therapeutic Applications of CRISPR/Cas9 Genome Editing in Breast Cancer.Genes · 2021Review
- Identification of Genes Required for Enzalutamide Resistance in Castration-Resistant Prostate Cancer CellsMolecular cancer therapeutics · 2021Article
- Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma.World journal of gastroenterology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed-lineage kinase 3 (MLK3) was first cloned in 1994; however, only in the past decade has MLK3 become recognized as a player in oncogenic signaling. MLK3 is a mitogen-activated protein kinase kinase kinase (MAP3K) that mediates signals from several cell surface receptors including receptor tyrosine kinases (RTKs), chemokine receptors, and cytokine receptors. Once activated, MLK3 transduces signals to multiple downstream pathways, primarily to c-Jun terminal kinase (JNK) MAPK, as well as to extracellular-signal-regulated kinase (ERK) MAPK, P38 MAPK, and NF-κB, resulting in both transcriptional and post-translational regulation of multiple effector proteins. In several types of cancer, MLK3 signaling is implicated in promoting cell proliferation, as well as driving cell migration, invasion and metastasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.