ArticleJournal of translational medicine2025
Molecule interacting with CasL-2 enhances tumor progression and alters radiosensitivity in cervical cancer.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Molecular Biomarkers of Radiosensitivity and Radioresistance in Cervical Cancer: A Systematic Review.International journal of molecular sciences · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveCervical cancer is a common malignancy among women, and radiotherapy remains a primary treatment modality across all disease stages. However, resistance to radiotherapy frequently results in treatment failure, highlighting the need to identify novel therapeutic targets to improve clinical outcomes.
methodsThe expression of molecule interacting with CasL-2 (MICAL2) was confirmed in cervical cancer tissues and cell lines through western blotting (WB) and immunohistochemistry (IHC). Siha and Hela cells were used to examine the regulatory and biological functions of MICAL2 via knockdown and overexpression experiments. Assays including MTT, colony formation, wound healing, transwell migration, and sphere formation were employed, along with WB analysis. DNA damage in irradiated cells with MICAL2 knockdown or overexpression was evaluated using the comet assay, while γ-H2AX and Rad51 protein levels were detected by WB. In vivo experiments validated the tumorigenic and radioresistance functions of MICAL2. Additionally, the relationship between MICAL2 expression and radiotherapy response was analyzed in 62 patients with cervical cancer by assessing tumor regression and MICAL2 levels six months post-treatment.
resultsMICAL2 expression was significantly elevated in cervical cancer tissues and cells. Functional analyses demonstrated that MICAL2 promotes cell proliferation, migration, and invasion by activating the MAPK and PI3K/AKT pathways, as confirmed through both in vitro and in vivo experiments. Silencing MICAL2 increased DNA damage, impeded DNA repair, and enhanced radiosensitivity. Among the 62 patients with cervical cancer, elevated MICAL2 expression was associated with a lower complete response rate to radiotherapy (25.6% vs. 60.9% in those with low expression), reduced progression-free survival, and advanced cancer stage (*p < 0.05).
conclusionMICAL2 plays a critical role in tumor progression and radiotherapy resistance in cervical cancer. These findings provide a foundation for developing targeted therapies to improve treatment outcomes in this population.
Indexed as
Identifiers
What 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.