ArticleCell death & disease2025
Hypomethylation induced overexpression of PLOD3 facilitates colorectal cancer progression through TM9SF4-mediated autophagy.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 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
6 citing papers in PubMed.
- Hypoxia-induced PLOD3 activates the NEDD4/GOT2 axis to exacerbate renal cell carcinoma progression.Cell death & disease · 2026Article
- Genome-wide extraction of differentially methylated DNA regions using adapter-anchored proximity primers.Nucleic acids research · 2026Article
- Serum DIP2C protein concentration in human colorectal cancer among Yemeni patients.Frontiers in oncology · 2026Article
- Structure-based design of new potent and highly selective PARP-1 inhibitor for treating colorectal cancer.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 2025Review
- Research Advances of the Autophagy-Regulated Radiosensitivity.Cell proliferation · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Colorectal cancer (CRC) ranks among the primary causes of human mortality globally. Numerous studies have highlighted the significant role of PLOD3 in the progression of various cancers. However, the exact function and underlying mechanisms of PLOD3 in CRC remains incompletely understood. To investigate the expression of PLOD3, qRT‒PCR, immunohistochemistry and western blotting were utilized to analyze the expression of PLOD3 in CRC tissues and adjacent normal tissues. Functional assays were conducted to assess the roles of PLOD3 both in vitro and in vivo. To elucidate the potential mechanism of PLOD3 in CRC, a range of techniques, including coimmunoprecipitation, immunofluorescence, CHX pulse-chase, and ubiquitination assays were used. As the results indicated, hypomethylation of the PLOD3 promoter leads to its over- expression in CRC, and elevated PLOD3 levels are associated with a poor prognosis. Both in vitro and in vivo models demonstrated that PLOD3 enhances CRC cell proliferation, invasion, and migration. Furthermore, through mechanistic studies, TM9SF4 was identified as a protein that interacts with PLOD3 and contributes to CRC progression by promoting autophagy. Additionally, PLOD3 could be secreted by CRC cells and secreted PLOD3 could promote CRC cells migration and invasion. These results demonstrated that PLOD3 promotes CRC progression through the PLOD3/TM9SF4 axis and could be a potential biomarker and treatment target 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.