ArticleOncogene2011
Sds22/PP1 links epithelial integrity and tumor suppression via regulation of myosin II and JNK signaling.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- High-throughput mechanomic screening reveals novel regulators of single-cell mechanics.Biophysical journal · 2026Article
- SDS22 coordinates the assembly of holoenzymes from nascent protein phosphatase-1.Nature communications · 2024Article
- Article
- Article
- Exploiting codon usage identifies intensity-specific modifiers of Ras/MAPK signaling in vivo.PLoS genetics · 2020Article
- Protein Phosphatase 1 Regulatory Subunit SDS22 Inhibits Breast Cancer Cell Tumorigenesis by Functioning as a Negative Regulator of the AKT Signaling Pathway.Neoplasia (New York, N.Y.) · 2019Article
- Modelling Cooperative Tumorigenesis inBioMed research international · 2018Review
- The Drosophila Imaginal Disc Tumor Model: Visualization and Quantification of Gene Expression and Tumor Invasiveness Using Genetic Mosaics.Journal of visualized experiments : JoVE · 2016Article
- The Fra-1-miR-134-SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells.Cell death & disease · 2016Article
- Review
- Interplay among Drosophila transcription factors Ets21c, Fos and Ftz-F1 drives JNK-mediated tumor malignancy.Disease models & mechanisms · 2015Article
- Article
- Mineralocorticoid receptor interaction with SP1 generates a new response element for pathophysiologically relevant gene expression.Nucleic acids research · 2013Article
- In Drosophila, RhoGEF2 cooperates with activated Ras in tumorigenesis through a pathway involving Rho1-Rok-Myosin-II and JNK signalling.Disease models & mechanisms · 2013Article
- Interaction proteome of human Hippo signaling: modular control of the co-activator YAP1.Molecular systems biology · 2013Article
- Suppressors of ipl1-2 in components of a Glc7 phosphatase complex, Cdc48 AAA ATPase, TORC1, and the kinetochore.G3 (Bethesda, Md.) · 2012Article
- Gene expression profiling of peripheral blood mononuclear cells in the setting of peripheral arterial disease.Journal of clinical bioinformatics · 2012Article
- Nutrient limitations alter cell division control and chromosome segregation through growth-related kinases and phosphatases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Modeling tumor invasion and metastasis in Drosophila.Disease models & mechanisms · 2011Review
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 1 institution in 1 country.
Funding
Abstract
Loss of epithelial integrity often correlates with the progression of malignant tumors. Sds22, a regulatory subunit of protein phosphatase 1 (PP1), has recently been linked to regulation of epithelial polarity in Drosophila. However, its role in tumorigenesis remains obscure. In this study, using Drosophila imaginal tissue as an in vivo model system, we show that sds22 is a new potential tumor suppressor gene in Drosophila. Without sds22, cells lose epithelial architecture, and become invasive and tumorigenic when combined with Ras overexpression; conversely, sds22 overexpression can largely suppress tumorigenic growth of Ras(V12)scrib(-/-) mutant cells. Mechanistically, we show that sds22 prevents cell invasion and metastasis by inhibiting myosin II and Jun N-terminal kinase (JNK) activity downstream of PP1. Loss of this inhibition causes cells to lose epithelial organization and promotes cell invasion. Finally, human Sds22 is focally deleted and downregulated in multiple carcinomas, and this downregulation correlates with tumor progression, suggesting that sds22 inactivation may contribute to tumorigenesis and metastatic potential in human cancers via a similar mechanism.
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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.