ReviewOncotarget2016
AKT-ions with a TWIST between EMT and MET.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 93 citations in OpenAlex.
- Repurposing ramipril to mitigate EMT-like transition in endometriosis by PI3K/AKT/S6K1 signalling pathway: a study in endometriosis induced rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Tumour necrosis factor receptor-associated factor 7 drives leukaemogenesis through the TWIST1-P2RX1-CaJournal of translational medicine · 2026Article
- The ATM inhibitor KU55933 inhibits TGF-β1-mediated epithelial to mesenchymal transition in colorectal cancer cells.Frontiers in oncology · 2026Article
- The influence of menstrual cycle and endometriosis on endometrial expression of epithelial-to-mesenchymal transition (EMT)-related genes.Reproductive biology and endocrinology : RB&E · 2025Article
- S100 Calcium-Binding Protein P and Cathepsin E as Key Mediators in Pancreatic Cancer Tumorigenesis.Biomedicines · 2025Article
- Reciprocal Modulation of Tumour and Immune Cell Motility: Uncovering Dynamic Interplays and Therapeutic Approaches.Cancers · 2025Review
- Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Fibroblasts Regulate the Transformation Potential of Human Papillomavirus-positive Keratinocytes.bioRxiv : the preprint server for biology · 2024Article
- Single-cell transcriptional signature-based drug repurposing and in vitro evaluation in colorectal cancer.BMC cancer · 2024Article
- Review
- PTEN depletion reduces H3K27me3 levels to promote epithelial-to-mesenchymal transition in epithelial colorectal cancer cells.PloS one · 2024Article
- Defining the Role of Metastasis-Initiating Cells in Promoting Carcinogenesis in Ovarian Cancer.Biology · 2023Review
- Oxidative stress regulation and related metabolic pathways in epithelial-mesenchymal transition of breast cancer stem cells.Stem cell research & therapy · 2023Review
- The role and function of CLU in cancer biology and therapy.Clinical and experimental medicine · 2023Review
- Role of pelitinib in the regulation of migration and invasion of hepatocellular carcinoma cells via inhibition of Twist1.BMC cancer · 2023Article
- The Role of PRMT5 in Immuno-Oncology.Genes · 2023Review
- Hedgehog signaling regulates the development and treatment of glioblastoma.Oncology letters · 2022Review
- Molecular mechanism of CD163Annals of translational medicine · 2022Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor Twist is an important regulator of cranial suture during embryogenesis. Closure of the neural tube is achieved via Twist-triggered cellular transition from an epithelial to mesenchymal phenotype, a process known as epithelial-mesenchymal transition (EMT), characterized by a remarkable increase in cell motility. In the absence of Twist activity, EMT and associated phenotypic changes in cell morphology and motility can also be induced, albeit moderately, by other transcription factor families, including Snail and Zeb. Aberrant EMT triggered by Twist in human mammary tumour cells was first reported to drive metastasis to the lung in a metastatic breast cancer model. Subsequent analysis of many types of carcinoma demonstrated overexpression of these unique EMT transcription factors, which statistically correlated with worse outcome, indicating their potential as biomarkers in the clinic. However, the mechanisms underlying their activation remain unclear. Interestingly, increasing evidence indicates they are selectively activated by distinct intracellular kinases, thereby acting as downstream effectors facilitating transduction of cytoplasmic signals into nucleus and reprogramming EMT and mesenchymal-epithelial transition (MET) transcription to control cell plasticity. Understanding these relationships and emerging data indicating differential phosphorylation of Twist leads to complex and even paradoxical functionalities, will be vital to unlocking their potential in clinical settings.
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.