ArticleHistology and histopathology2026
FAM107A inhibits Invasion and migration of colorectal cancer by affecting EMT via the AKT pathway.
Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Metastasis of colorectal cancer (CRC) is the main cause of CRC-related mortality. FAM107A is widely expressed in various normal tissues. However, few studies have revealed the biological function of FAM107A in epithelial-mesenchymal transition (EMT) in human cancer cells, and the related molecular mechanisms and signaling cascades are completely unknown. Here, we found that FAM107A was abnormally expressed in human CRC tissues and cell lines. Further research has shown that overexpression of FAM107A through transfection weakened the expression level of EMT-related markers. In addition, our research results indicated that upregulation of FAM107A inhibited the AKT signaling cascade in human CRC cells, while AKT activators restored activation of p50, indicating that FAM107A may regulate EMT through AKT activation of p50. Our results suggest that FAM107A could be a potential target for the treatment of CRC.
Indexed as
Identifiers
41363049What 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.