ArticleThe Journal of biological chemistry2016
The Small C-terminal Domain Phosphatase 1 Inhibits Cancer Cell Migration and Invasion by Dephosphorylating Ser(P)68-Twist1 to Accelerate Twist1 Protein Degradation.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- UCHL1 stabilizes Twist1 via K11/K63-linked deubiquitination to drive tumor metastasis in non-small cell lung cancer.Cell death discovery · 2025Article
- Retinoic acid induced specific changes in the phosphoproteome of C17.2 neural stem cells.Journal of cellular and molecular medicine · 2024Article
- Molecular mechanisms of TWIST1-regulated transcription in EMT and cancer metastasis.EMBO reports · 2023Article
- Tumor Suppressor Properties of Small C-Terminal Domain Phosphatases in Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2023Article
- Investigation of Flavonoid Scaffolds as DAX1 Inhibitors against Ewing Sarcoma through Pharmacoinformatic and Dynamic Simulation Studies.International journal of molecular sciences · 2023Article
- MiR-574-5p promotes cell proliferation by negatively regulating small C-terminal domain phosphatase 1 in esophageal squamous cell carcinoma.Iranian journal of basic medical sciences · 2022Article
- Epithelial-Mesenchymal Transition by Synergy between Transforming Growth Factor-β and Growth Factors in Cancer Progression.Diagnostics (Basel, Switzerland) · 2022Review
- Angiotensin-(1-7) ameliorates high glucose-induced vascular endothelial injury through suppressing chloride channel 3.Bioengineered · 2022Article
- The Post-Translational Regulation of Epithelial-Mesenchymal Transition-Inducing Transcription Factors in Cancer Metastasis.International journal of molecular sciences · 2021Review
- ZNF451 stabilizes TWIST2 through SUMOylation and promotes epithelial-mesenchymal transition.American journal of cancer research · 2021Article
- Twist1: A Double-Edged Sword in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2020Review
- Targeting the C-Terminal Domain Small Phosphatase 1.Life (Basel, Switzerland) · 2020Review
- Tumor suppressor properties of the small C-terminal domain phosphatases in non-small cell lung cancer.Bioscience reports · 2019Article
- TWIST1 Heterodimerization with E12 Requires Coordinated Protein Phosphorylation to Regulate Periostin Expression.Cancers · 2019Article
- Effects of SIRT1 silencing on viability, invasion and metastasis of human glioma cell lines.Oncology letters · 2019Article
- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Expression signature of ten genes predicts the survival of patients with estrogen receptor positive-breast cancer that were treated with tamoxifen.Oncology letters · 2018Article
- Two-track virtual screening approach to identify both competitive and allosteric inhibitors of human small C-terminal domain phosphatase 1.Journal of computer-aided molecular design · 2017Article
- FGFR signaling maintains a drug persistent cell population following epithelial-mesenchymal transition.Oncotarget · 2016Article
- AKT-ions with a TWIST between EMT and MET.Oncotarget · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Twist1 is a basic helix-loop-helix transcription factor that strongly promotes epithelial-to-mesenchymal transition, migration, invasion, and metastasis of cancer cells. The MAPK-phosphorylated Twist1 on its serine 68 (Ser(P)(68)-Twist1) has a significantly enhanced stability and function to drive cancer cell invasion and metastasis. However, the phosphatase that dephosphorylates Ser(P)(68)-Twist1 and destabilizes Twist1 has not been identified and characterized. In this study, we screened a serine/threonine phosphatase cDNA expression library in HEK293T cells with ectopically coexpressed Twist1. We found that the small C-terminal domain phosphatase 1 (SCP1) specifically dephosphorylates Ser(P)(68)-Twist1 in both cell-free reactions and living cells. SCP1 uses its amino acid residues 43-63 to interact with the N terminus of Twist1. Increased SCP1 expression in cells decreased Ser(P)(68)-Twist1 and total Twist1 proteins, whereas knockdown of SCP1 increased Ser(P)(68)-Twist1 and total Twist1 proteins. Furthermore, the levels of SCP1 are negatively correlated with Twist1 protein levels in several cancer cell lines. SCP1-dephosphorylated Twist1 undergoes fast degradation via the ubiquitin-proteasome pathway. Importantly, an increase in SCP1 expression in breast cancer cells with either endogenous or ectopically expressed Twist1 largely inhibits the Twist1-induced epithelial-to-mesenchymal transition phenotype and the migration and invasion capabilities of these cells. These results indicate that SCP1 is the phosphatase that counterregulates the MAPK-mediated phosphorylation of Ser(68)-Twist1. Thus, an increase in SCP1 expression and activity may be a useful strategy for eliminating the detrimental roles of Twist1 in cancer cells.
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Registered trials
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