ArticleAmerican journal of cancer research2022
δ-Catenin promotes cell migration and invasion via Bcl-2-regulated suppression of autophagy in prostate cancer cells.
Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Novel role of LLGL2 silencing in autophagy: reversing epithelial-mesenchymal transition in prostate cancer.Biological research · 2024Article
- Atg5 knockout induces alternative autophagy via the downregulation of Akt expression.Toxicological research · 2023Article
- Differences in the pathogenetic characteristics of prostate cancer in the transitional and peripheral zones and the possible molecular biological mechanisms.Frontiers in oncology · 2023Review
- Delta-Catenin as a Modulator of Rho GTPases in Neurons.Frontiers in cellular neuroscience · 2022Review
- MicroRNA-122 targets δ-catenin to suppress the tumorigenic potential of prostate cancer cells.American journal of cancer research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a member of the catenin family, δ-catenin is overexpressed in many cancers, including prostate cancer, and the role of δ-catenin in prostate tumor growth has been reported. However, the involvement of δ-catenin in the migration and invasion of prostate cancer has rarely been studied. In this study, we innovatively proposed that δ-catenin would enhance the migration and invasion ability of prostate cancer cells. It is worth noting that the molecular mechanism underlying the effect involved the downregulation of autophagy. We demonstrated that δ-catenin could suppress autophagy by Bcl-2-regulated disruption of the Beclin1-Vps34 autophagosome complex. Furthermore, the effect of δ-catenin on promoting cell migration and invasion was dependent upon β-catenin-mediated Bcl-2 transcription. Finally, using rapamycin and bafilomycin, we largely confirmed that the degradation of Snails by autolysosomes may be related to δ-catenin regulated migration and invasion. Overall, our results indicated that δ-catenin promoted cell migration and invasion of prostate cancer cells via Bcl-2-regulated autophagy suppression.
Indexed as
Identifiers
35141007PMC8822292W4211266949What 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.