ArticleCancer cell international2025
Suppression of pentraxin 3 inhibits human osteosarcoma cell metastasis by repressing MAZ through STAT3 pathway.
Article in Cancer cell international, 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.
- PTX3 facilitates tumor cell migration and invasion through the miR-1255b-2-3p/CYP2J2 axis in oral squamous cell carcinoma.Cancer cell international · 2026Article
- Narciclasine triggers apoptosis in osteosarcoma cells via JNK-mediated extrinsic and intrinsic pathways.International journal of medical sciences · 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
7 authors.
Funding
Abstract
backgroundPentraxin 3 (PTX3), also known as TNF-inducible gene 14 protein (TSG-14), exerts pleiotropic roles in inflammation, immune responses, and a myriad of cancers, but there is limited knowledge regarding the role of PTX3 in the metastasis of human osteosarcoma.
methodsUsing RNA sequencing technology, transfection, western blotting, flow cytometry, and luciferase reporter, colony formation, quantitative reverse transcription–polymerase chain reaction (qRT-PCR), boyden chamber assays, and a xenograft model, the effects of PTX3 on cell migration and invasion in human osteosarcoma cells were investigated.
resultsPTX3 silencing repressed migration and invasion in U-2OS cells and PTX3 overexpression accelerated migration and invasion in HOS cells. Recombinant human PTX3 (rhPTX3) increased migration and invasion of HOS cells. In PTX3 knockdown U-2OS cells, the heatmap revealed the downregulation of Myc-associated zinc finger protein (MAZ), which is associated with the epithelial-mesenchymal transition pathway and osteosarcoma tissues. MAZ overexpression rescued the inhibition of migration by PTX3 knockdown in osteosarcoma cells. The activity of the MAZ promoter was reduced with PTX3 knockdown in osteosarcoma cells. While Stat3 overexpression rescued the inhibition of MAZ expression and migration by PTX3 knockdown in osteosarcoma cells. Moreover, in tail vein injection experiments, shPTX3 U-2OS cells reduced pulmonary metastasis formation in immunodeficient nude mice. By repressing MAZ through Stat3, suppression of PTX3 inhibits migration and invasion in osteosarcoma cells, and knockdown of PTX3 reduces pulmonary metastasis.
conclusionsOur results raise interest in further study of PTX3’s anti-metastasis properties in osteosarcoma, providing molecular insight into PTX3’s role in osteosarcoma metastasis.
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.