ArticleEuropean journal of medical research2025
Therapeutic efficacy of 5-alkylresorcinol on progression of colorectal cancer by activating HCLS1 and suppressing TLR4/MYD88/NF-κB signaling.
Article in European journal of medical research, 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.
- Article
- FOXK1 drives colorectal cancer progression by transcriptionally activating GRB2.European journal of medical research · 2025Article
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
backgroundThis study investigates the molecular mechanisms underlying the inhibitory effects of 5-alkylresorcinol (5ARs) on colorectal cancer (CRC) growth.
methodsHCT116 cells were treated with 15 μmol/L 5ARs for 24 h, with both control and 5ARs-treated groups undergoing transcriptome sequencing. Hub genes were identified through GO and KEGG enrichment analyses. Construct the overexpression plasmid and interference plasmid of HCLS1, and transfect them into HCT116 cells. The impact of HCLS1 on 5ARs' therapeutic effect was evaluated using CCK-8, RT-qPCR, and WB assays. Subsequent animal experiments involved the application of BALB/c nude mice which were injected with HCT116 cells. Three groups were formed: model, 5ARs treatment, and 5ARs treatment with adeno-associated virus (AAV) overexpression plasmid of HCLS1. Tumor growth, Ki67 proliferation, and gene expression were assessed.
resultsDEGs were primarily enriched in the regulation of myeloid cell differentiation and tight junction, from which the HCLS1 gene exhibiting the highest fold change was selected as the candidate gene. 5ARs significantly increased HCLS1 expression and inhibited TLR4/MYD88/NF-κB (p-p65) expression. Both cellular and animal experiments showed 5ARs and HCLS1 overexpression inhibited HCT116 cell proliferation, tumor growth and TLR4/MYD88/NF-κB (p-p65) expression.
conclusionsThese findings suggest that 5ARs may exert their anti-cancer effects by activating HCLS1 and suppressing TLR4/MYD88/NF-κB signaling, thus offering a potential new therapeutic strategy for 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.