ArticleCancer medicine2025
ASAP1 Promotes Epithelial to Mesenchymal Transition by Activating the TGFβ Pathway in Papillary Thyroid Cancer.
Article in Cancer medicine, 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
- ASAP1 Promotes Epithelial to Mesenchymal Transition by Activating the TGFβ Pathway in Papillary Thyroid Cancer.Cancer medicine · 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
8 authors.
Funding
Abstract
backgroundPapillary thyroid cancer (PTC) is the most common type of thyroid malignancy. While the prognosis of PTC is generally favorable, some cases exhibit aggressive behavior, leading to metastasis and recurrence. ASAP1 (ArfGAP with SH3, ankyrin repeats, and PH domain 1), an ADP-ribosylation factor GTPase-activating protein, has been implicated in tumor metastasis. However, its role in PTC remains unclear.
methodsASAP1 expression in PTC was evaluated using TCGA and GEO databases. Studies in PTC cell lines (MDA-T32 and MDA-T85) included lentiviral-mediated knockdown and overexpression of ASAP1 to assess effects on epithelial-mesenchymal transition (EMT) marker expression, cell proliferation, and invasive capacity. TGFβ pathway activity was examined by p-SMAD2 Western blotting and luciferase reporter assays. ASAP1-SMAD2/3 interactions were analyzed using co-immunoprecipitation (CO-IP) and immunofluorescence.
resultsASAP1 was aberrantly upregulated in PTC. Lentiviral knockdown of ASAP1 in PTC cells suppressed the EMT process. Reduced ASAP1 expression also inhibited cell survival, proliferation, migration, invasion, and the expression of p-SMAD2 in the TGFβ pathway in PTC cells. Conversely, ASAP1 overexpression reversed these effects. Mechanistically, ASAP1 interacts with the SMAD2/3 complex, forming a positive feedback loop with TGFβ signaling that promotes EMT and cell invasiveness in PTC cells, which suggests its potential role in PTC metastasis.
conclusionsThese findings suggest that targeting ASAP1 may offer a novel therapeutic strategy to limit PTC metastasis by suppressing EMT and attenuating the TGFβ pathway.
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.