ArticleCell death & disease2026
Semaphorin 6D drives anti-tumor type I interferon responses to reprogram the tumor microenvironment in colorectal cancer.
Article in Cell death & disease, 2026. 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
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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.
- Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026Review
- Acidosis promotes exon skipping through sequestering SR-rich splicing factors in nuclear speckles.Frontiers in molecular biosciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Colorectal cancer (CRC) persists as the third most prevalent cause of cancer-associated mortality worldwide, largely due to late diagnosis, limited treatment efficacy, and poor response to immunotherapy. However, the underlying molecular mechanisms remain incompletely characterized. This study identified Semaphorin 6D (SEMA6D) as a potential tumor suppressor that was markedly underexpressed in CRC and associated with poor prognosis. Promoter hypermethylation emerges as the primary mechanism underlying its transcriptional silencing, with notably low expression observed in CIMP-H, MSI-H, CMS4 and CMS1 subtypes. Functional experiments demonstrated that SEMA6D overexpression significantly attenuated cellular proliferation, epithelial-mesenchymal transition (EMT), and migratory capacity in vitro, while concurrently suppressing tumor growth and metastatic spread in vivo. Conversely, SEMA6D depletion induced pro-tumorigenic phenotypes. Moreover, SEMA6D enhanced anti-tumor immunity by enhancing the infiltration of CD4
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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 Socratic graph.