ArticleCell death & disease2018
U-box ubiquitin ligase PPIL2 suppresses breast cancer invasion and metastasis by altering cell morphology and promoting SNAI1 ubiquitination and degradation.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- E3 Ubiquitin Ligases in Breast Cancer Metastasis: A Systematic Review of Pathogenic Functions and Clinical Implications.Frontiers in oncology · 2021Pooled it
- FBXO28 targets SNAI1 for ubiquitin-proteasomal degradation in non-small cell lung cancer.The Journal of biological chemistry · 2026Article
- PPIL2 suppression induces cellular senescence and inhibits proliferation in hepatocellular carcinoma via c-myc/p21 axis.The Journal of biological chemistry · 2026Article
- Structural and Kinetic Variability of Pathogen Cyclophilins: Functional Diversification and Therapeutic Potential.ACS infectious diseases · 2026Review
- Human Cyclophilins-An Emerging Class of Drug Targets.Medicinal research reviews · 2026Review
- Regulatory mechanisms for Snail protein stability: ubiquitin-proteasome system and chaperone-mediated autophagy.Experimental & molecular medicine · 2026Review
- PPIL2 is a target of the JAK2/STAT5 pathway and promotes myeloproliferation via degradation of p53.The Journal of clinical investigation · 2025Article
- Genetic feature selection algorithm as an efficient glioma grade classifier.Scientific reports · 2025Article
- Control of Snail1 protein stability by post-translational modifications: the basis for a complex regulation of Snail1 function.International journal of biological sciences · 2025Review
- HPV, HBV, and HIV-1 Viral Integration Site Mapping: A Streamlined Workflow from NGS to Genomic Insights of Carcinogenesis.Viruses · 2024Article
- MARCH2, a Novel Oncogene-regulated SNAIL E3 Ligase, Suppresses Triple-negative Breast Cancer Metastases.Cancer research communications · 2024Article
- Ubiquitin-specific Protease 35 Promotes Gastric Cancer Metastasis by Increasing the Stability of Snail1.International journal of biological sciences · 2024Article
- Relationship between the Ubiquitin-Proteasome System and Autophagy in Colorectal Cancer Tissue.Biomedicines · 2023Article
- USP36 stabilizes nucleolar Snail1 to promote ribosome biogenesis and cancer cell survival upon ribotoxic stress.Nature communications · 2023Article
- Downregulated circPOKE promotes breast cancer metastasis through activation of the USP10-Snail axis.Oncogene · 2023Article
- p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism.Nature communications · 2023Article
- USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- KLF12 promotes the proliferation of breast cancer cells by reducing the transcription of p21 in a p53-dependent and p53-independent manner.Cell death & disease · 2023Article
- Differential gene expression of immunity and inflammation genes in colorectal cancer using targeted RNA sequencing.Frontiers in oncology · 2023Article
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Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is the leading cause of breast cancer fatalities. To develop new therapeutic strategies, the mechanisms underlying breast cancer invasion and metastasis need to be further investigated. Peptidylprolyl isomerase (cyclophilin)-like 2 (PPIL2) is a U-box-type E3 ubiquitin ligase belonging to the cyclophilin family. Proteins within this family are the major cytosolic binding proteins of the immunosuppressant drug cyclosporine A (CsA). Although PPIL2 has been reported to potentially be involved in cell migration, its role in breast cancer is still unclear. Herein, we demonstrate that PPIL2 suppressed metastasis in a breast cancer model by altering cell morphology and suppressing the epithelial-mesenchymal transition (EMT) process. Moreover, elevated PPIL2 inhibited EMT and breast cancer invasion by interacting with the classical EMT transcription factor, SNAI1, to enhance its ubiquitin-dependent degradation. Furthermore, PPIL2 protein level and stability was upregulated after CsA treatment, indicating that PPIL2 might be involved in CsA-mediated repression of EMT in breast cancer. Analysis of tissue samples taken from breast cancer patients showed a significant correlation between the expression of PPIL2 and the degree of cancer invasion and metastasis. In summary, these results would shed light on a potential clinical use of CsA in breast cancer patients.
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