ArticleCell and tissue research2025
Downregulation of ankyrin 3 (ANK3) promotes malignant behaviors associated with altered adhesion dynamics and actin cytoskeleton remodeling in renal cell carcinoma.
Article in Cell and tissue research, 2025. 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
14 authors.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer, with existing therapies largely ineffective for advanced stages. Ankyrin 3 (ANK3), a protein involved in various cellular processes, has been associated with poor prognosis and immune infiltration in ccRCC. However, its role in ccRCC development and progression remains poorly understood. In the present study, ANK3-knockdown 786-O cells were generated using a shRNA approach. Cellular assays revealed that ANK3 knockdown significantly enhanced cell proliferation, migration, and invasion compared to shControl cells. ANK3-knockdown cells also displayed increased nuclear size and accumulation of G2/M phase of the cell cycle. Proteomic analysis identified 59 significantly altered proteins in ANK3-knockdown cells, primarily involved in cell adhesion and structural integrity. Among these, 10 proteins were significantly associated with overall survival in ccRCC patients. Morphological analysis showed that ANK3-knockdown cells exhibited a more spindle-like shape and increased cellular protrusions (filopodia). Western blot analysis further demonstrated altered expression levels of junctional and cytoskeleton proteins, including decreased E-cadherin and increased ZO-1, ICAM-1, vimentin, and β-actin. Immunofluorescence analysis revealed the accumulation of F-actin in the cytoplasm and filopodia in ANK3-knockdown cells. Additionally, ANK3 knockdown enhanced cell adhesion and aggregation capabilities. Finally, a decrease in ANK3 expression was confirmed in ccRCC tissues (grades I and II) compared to adjacent normal tissues. These findings suggest that ANK3 acts as a potential modulator of cell adhesion and cytoskeleton remodeling in ccRCC and may represent a promising therapeutic target for this malignancy.
Indexed as
Identifiers
41186628What 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.