ArticleOncotarget2016
MICAL2 is a novel human cancer gene controlling mesenchymal to epithelial transition involved in cancer growth and invasion.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The trial behind it
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Unraveling the dual roles of MICAL2 in skeletal muscle physiology and fusion negative rhabdomyosarcoma tumor progression.Cell death & disease · 2026Article
- miR-6850 drives phenotypic changes and signaling in high grade serous ovarian cancer.Non-coding RNA research · 2026Article
- miR‑205: A dual regulator of angiogenesis in health and disease (Review).International journal of molecular medicine · 2026Review
- Article
- LncRNANon-coding RNA research · 2025Article
- Analysis of Microarray and Single-Cell RNA-Seq Finds Gene Co-Expression and Tumor Environment Associated with Extracellular Matrix in Epithelial-Mesenchymal Transition in Prostate Cancer.International journal of molecular sciences · 2025Article
- Structural insights into the roles of PARP4 and NADNature communications · 2025Article
- Redox and actin, a fascinating story.Redox biology · 2025Review
- Molecular pathological approach to cancer epigenomics and its clinical application.Pathology international · 2024Review
- MICAL2 implies immunosuppressive features and acts as an independent and adverse prognostic biomarker in pancreatic cancer.Scientific reports · 2024Article
- Article
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway.Cell communication and signaling : CCS · 2022Article
- Copy number alterations and epithelial‑mesenchymal transition genes in diffuse and intestinal gastric cancers in Mexican patients.Molecular medicine reports · 2022Article
- Phosphorylation of MICAL2 by ARG promotes head and neck cancer tumorigenesis by regulating skeletal rearrangement.Oncogene · 2022Article
- Microgravity and space radiation inhibit autophagy in human capillary endothelial cells, through either opposite or synergistic effects on specific molecular pathways.Cellular and molecular life sciences : CMLS · 2021Article
- Enriching the Arsenal of Pharmacological Tools against MICAL2.Molecules (Basel, Switzerland) · 2021Article
- MICAL2PV suppresses the formation of tunneling nanotubes and modulates mitochondrial trafficking.EMBO reports · 2021Article
- Conserved human effector Treg cell transcriptomic and epigenetic signature in arthritic joint inflammation.Nature communications · 2021Article
- CRISPR/Cas9-Mediated Whole Genomic Wide Knockout Screening Identifies Specific Genes Associated With PMFrontiers in bioengineering and biotechnology · 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
16 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MICAL (Molecules Interacting with CasL) proteins catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. Here we show for the first time that MICAL2 mRNA is significantly over-expressed in aggressive, poorly differentiated/undifferentiated, primary human epithelial cancers (gastric and renal). Immunohistochemistry showed MICAL2-positive cells on the cancer invasive front and in metastasizing cancer cells inside emboli, but not at sites of metastasis, suggesting MICAL2 expression was 'on' in a subpopulation of primary cancer cells seemingly detaching from the tissue of origin, enter emboli and travel to distant sites, and was turned 'off' upon homing at metastatic sites. In vitro, MICAL2 knock-down resulted in mesenchymal to epithelial transition, reduction of viability, and loss of motility and invasion properties of human cancer cells. Moreover, expression of MICAL2 cDNA in MICAL2-depleted cells induced epithelial to mesenchymal transition. Altogether our data indicate that MICAL2 over-expression is associated with cancer progression and metastatic disease. MICAL2 might be an important regulator of epithelial to mesenchymal transition and therefore a promising target for anti-metastatic therapy.
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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.