ArticleDiscover oncology2026
DNMT1 promotes the malignant progression of colorectal cancer by silencing HOXD11 via promoter hypermethylation.
Article in Discover oncology, 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
5 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is a prevalent malignancy worldwide, and epigenetic modifications, particularly methylation of key genes, play a crucial role in its initiation and progression. DNA methyltransferase 1 (DNMT1) is aberrantly overexpressed in CRC; however, its specific mechanisms of action and downstream targets remain unclear. This study aims to elucidate how DNMT1 epigenetically regulates HOXD11 expression and subsequently influences CRC progression.
methodsThe expression and methylation status of HOXD11 in 30 pairs of CRC tissues and adjacent normal tissues were detected by RT-qPCR, Western Blot, and methylation-specific PCR (MSP). HOXD11 overexpression assays were performed in CRC cell lines, and cell proliferation, migration, invasion, and apoptosis were evaluated using CCK-8, colony formation, wound healing, Transwell assays, and flow cytometry. To identify the key enzyme regulating HOXD11, we conducted specific shRNA knockdown screening of DNA methyltransferase family members (DNMT1, DNMT3A, and DNMT3B). The regulatory effect of DNMT1 on HOXD11 was then verified using the demethylating agent 5-AzaC. Finally, a nude mouse subcutaneous xenograft model was established to validate the therapeutic potential of targeting the DNMT1/HOXD11 axis in vivo.
resultsHOXD11 was significantly downregulated in CRC tissues, accompanied by promoter hypermethylation. Overexpression of HOXD11 markedly inhibited CRC cell proliferation, migration, and invasion, while inducing apoptosis. Mechanistic studies revealed that among the three DNMTs screened, only DNMT1 knockdown significantly upregulated HOXD11 expression, confirming DNMT1 as the specific methyltransferase mediating HOXD11 promoter hypermethylation and transcriptional silencing. Treatment with 5-AzaC restored HOXD11 expression and suppressed malignant phenotypes, whereas simultaneous knockdown of HOXD11 reversed these tumor-suppressive effects. In vivo experiments further confirmed that targeted inhibition of DNMT1 significantly curbed tumor growth by upregulating HOXD11.
conclusionThis study reveals that DNMT1-mediated promoter hypermethylation of HOXD11 is a critical mechanism driving the malignant progression of CRC. The DNMT1/HOXD11 axis may serve as a potential therapeutic target of CRC.
Indexed as
Identifiers
What 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.