ReviewInternational journal of molecular sciences2020
Regulation of Epithelial-to-Mesenchymal Transition by Alternative Translation Initiation Mechanisms and Its Implications for Cancer Metastasis.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 20 citations in OpenAlex.
- Predicting the Efficacy of Eribulin in Metastatic Breast Cancer by Assessing E-Cadherin and Vimentin Expression.Acta histochemica et cytochemica · 2025Article
- DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia.International journal of molecular sciences · 2024Article
- Regulating epithelial-mesenchymal plasticity from 3D genome organization.Communications biology · 2024Review
- Non-canonical mRNA translation initiation in cell stress and cancer.NAR cancer · 2024Review
- Breast cancer cell mesenchymal transition and metastasis directed by DAP5/eIF3d-mediated selective mRNA translation.Cell reports · 2023Article
- HIF-1α contributes to metastasis in choriocarcinoma by regulating DEC1 expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Therapeutic targeting approach on epithelial-mesenchymal plasticity to combat cancer metastasis.Medical oncology (Northwood, London, England) · 2023Review
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies.Frontiers in pharmacology · 2022Review
- LncRNAs and Chromatin Modifications Pattern mFrontiers in genetics · 2022Review
- Haploinsufficient tumor suppressor PRP4K is negatively regulated during epithelial-to-mesenchymal transition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Upregulation of CPNE7 in mesenchymal stromal cells promotes oral squamous cell carcinoma metastasis through the NF-κB pathway.Cell death discovery · 2021Article
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 2 institutions in 1 country.
Funding
Abstract
Translation initiation plays a critical role in the regulation of gene expression for development and disease conditions. During the processes of development and disease, cells select specific mRNAs to be translated by controlling the use of diverse translation initiation mechanisms. Cells often switch translation initiation from a cap-dependent to a cap-independent mechanism during epithelial-to-mesenchymal transition (EMT), a process that plays an important role in both development and disease. EMT is involved in tumor metastasis because it leads to cancer cell migration and invasion, and is also associated with chemoresistance. In this review we will provide an overview of both the internal ribosome entry site (IRES)-dependent and N
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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.