ArticleHuman cell2026
GATA6-mediated transcriptional activation and METTL3/IGF2BP2-dependent post-transcriptional stabilization upregulate CDC20 to promote the malignant progression of colorectal cancer and immune escape.
Article in Human cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) remains a leading cause of cancer mortality globally, underscoring the need to identify key molecular drivers. Cell division cycle 20 (CDC20), a regulator of cell cycle progression, is frequently dysregulated in malignancies. Its specific role and mechanisms in CRC pathogenesis are poorly understood, warranting investigation to uncover novel therapeutic targets. In this study, CDC20 mRNA expression was quantified by quantitative real-time polymerase chain reaction (qRT-PCR), while its protein levels were assessed using Western blotting. Cell proliferation was evaluated via the 5-Ethynyl-2'-deoxyuridine (EdU) assay. Cell apoptosis was analyzed by flow cytometry. Migration and invasion capabilities were examined using wound-healing and Transwell invasion assays, respectively. Angiogenesis was assessed using a tube formation assay. To investigate the in vivo effects of CDC20 knockdown, a xenograft mouse model was employed to monitor tumor growth. Flow cytometry was performed to quantify CD206( +) macrophages. Mechanistic studies included chromatin immunoprecipitation (ChIP), dual-luciferase reporter, RNA immunoprecipitation (RIP), and methylated RNA immunoprecipitation (MeRIP) assays to explore GATA binding protein 6 (GATA6) and methyltransferase-like 3 (METTL3) interactions with CDC20. The results showed that CDC20 expression at the mRNA and protein levels was significantly upregulated in CRC tissues in comparison with normal colorectal tissues. Moreover, its protein expression was higher in CRC cells than in human normal colonic epithelial cells. Its knockdown suppressed CRC cell proliferation, migration, invasion, and tube formation, while promoting apoptosis. In addition, CDC20 depletion inhibited tumor growth and immune escape. Transcription factor GATA6 directly activated transcription of the CDC20 gene. Crucially, restoring CDC20 expression counteracted the tumor-suppressive effects of GATA6 knockdown on malignant behaviors and immune escape. METTL3 stabilized CDC20 transcripts via insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)-mediated mRNA stability. Further, overexpressing CDC20 similarly reversed the inhibitory effects of METTL3 knockdown on CRC cell malignancy and immune escape. Thus, CDC20, upregulated transcriptionally by GATA6 and post-transcriptionally by METTL3, drove CRC progression, angiogenesis, and immune evasion. Targeting CDC20 or its regulators holds significant clinical promise for developing therapies in CRC patients.
Indexed as
Identifiers
42501233What 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.