ArticleFrontiers in oncology2025
DDX49 as a novel prognostic biomarker regulates colorectal cancer cell proliferation through the TIMM44-PI3K-AKT pathway.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
- Mechanistic study of TIMM44 mediating gastric carcinogenesis via the Gαi1-PI3K-AKT-mTOR signaling pathway.Scientific reports · 2026Article
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
No grant is acknowledged in the PubMed record.
Abstract
Objective: Colorectal cancer (CRC) ranks as the third most common global cancer. This study aims to explore the expression, function, and mechanism of DEAD-box helicase 49 (DDX49) in CRC. Methods: Pan-cancer data were obtained from The Cancer Genome Atlas (TCGA) database to compare expression differences of DDX49 across 33 types of cancers. Immunohistochemistry (IHC) was used to detect the protein expression levels of DDX49 in CRC. Kaplan-Meier curves and Cox proportional hazards regression model were employed to demonstrate the prognostic value of DDX49. The effects of key molecules on cancer cell proliferation were assessed using a Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Western blot (WB) was employed to measure key molecules in the PI3K-AKT pathway. Results: Both TCGA data and IHC showed that elevated DDX49 in CRC tumors was correlated with advanced stages and poor prognosis. DDX49 knockdown inhibited proliferation and colony formation in SW480 and HCT-8 cells, suppressing PI3K-AKT pathway activation and TIMM44 expression-reducing AKT phosphorylation. SC79 treatment partially rescued phosphorylated AKT and proliferation. TIMM44 knockdown mimicked these effects, while its overexpression restored AKT phosphorylation and proliferation in DDX49-knockdown cells. Conclusion: DDX49, a potential prognostic biomarker, promotes cell proliferation by TIMM44-PI3K-AKT pathway, which may offer a target for clinical anti-tumor therapy.
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.