ReviewHuman cell2025
The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.
Review in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- MICAL2 as a key effector of β-catenin signaling driving melanoma progression and therapeutic resistance.Cell death and differentiation · 2026Article
- Unraveling the dual roles of MICAL2 in skeletal muscle physiology and fusion negative rhabdomyosarcoma tumor progression.Cell death & disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attractive treatment strategy. Molecule interacting with CasL 2 (MICAL2) is a flavin protein monooxygenase family protein that interacts with CasL2 and is involved in cytoskeletal redox regulation, axon-directed regulation, cell transport, and apoptosis. MICAL2 induces F-actin depolymerization through REDOX modification, thereby promoting the expression of epithelial-mesenchymal transition (EMT)-related proteins and inducing cancer cell invasion and proliferation. Mechanistically, MICAL2 induces EMT by regulating the serum response factor (SRF)/myocardin-related transcription factor A (MRTF-A) signaling pathway, and the semaphorin/plexin pathway and inducing reactive oxygen species (ROS) production. Recent studies have shown that MICAL2 is highly expressed in tumors, accelerates tumor progression, and is a novel tumor-promoting factor. This article summarizes recent research findings to review the biological functions of MICAL2, the potential mechanisms related to cancer progression, and discusses the challenges and prospects in this area, providing a new theoretical basis for clinical molecular targeted therapy for cancer.
Indexed as
Identifiers
40240704What Socratic 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 Socratic graph.