ArticleOncotarget2015
p53 directly activates cystatin D/CST5 to mediate mesenchymal-epithelial transition: a possible link to tumor suppression by vitamin D3.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 54 citations in OpenAlex.
- Transcriptomic atlas of premalignant oral squamous cell carcinoma in an aging mouse model reveals an enhanced immune response and dysregulation of head and neck tissue stem cells.bioRxiv : the preprint server for biology · 2026Article
- Conserved stromal EMT program controls regenerative capacity of mesenchymal stromal cells across multiple tissues.Science advances · 2026Article
- Genetic and epigenetic determinants of vitamin D metabolism: nutrigenomic insights for precision nutrition.Frontiers in nutrition · 2026Review
- ITRAQ and PRM-based quantitative saliva proteomics in gastric cancer: biomarker discovery.Frontiers in molecular biosciences · 2025Article
- Investigation of CST7 and hsa-miR-4793-5p gene expression in breast cancer.Biochemistry and biophysics reports · 2024Article
- Immune cell signatures and inflammatory mediators: unraveling their genetic impact on chronic kidney disease through Mendelian randomization.Clinical and experimental medicine · 2024Article
- Type 2 Cystatins and Their Roles in the Regulation of Human Immune Response and Cancer Progression.Cancers · 2023Review
- Disease-related protein co-expression networks are associated with the prognosis of resectable node-positive pancreatic ductal adenocarcinoma.Scientific reports · 2022Article
- Gorham-Stout case report: a multi-omic analysis reveals recurrent fusions as new potential drivers of the disease.BMC medical genomics · 2022Article
- Impact of the interplay between stemness features, p53 and pol iota on replication pathway choices.Nucleic acids research · 2021Article
- Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.Cell & bioscience · 2021Article
- Vitamin D Enhances Radiosensitivity of Colorectal Cancer by Reversing Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2021Article
- Identification of Cysteine Protease Inhibitor CST2 as a Potential Biomarker for Colorectal Cancer.Journal of Cancer · 2021Article
- FOXA2-Interacting FOXP2 Prevents Epithelial-Mesenchymal Transition of Breast Cancer Cells by Stimulating E-Cadherin and PHF2 Transcription.Frontiers in oncology · 2021Article
- Interactions between the gut microbiome and host gene regulation in cystic fibrosis.Genome medicine · 2020Article
- Up-regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF-κB pathway.Journal of cellular and molecular medicine · 2019Article
- Collaboration of MYC and RUNX2 in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.Journal of cellular biochemistry · 2019Article
- The Role of Cysteine Cathepsins in Cancer Progression and Drug Resistance.International journal of molecular sciences · 2019Review
- Cystatin F as a key family 2 cystatin subunit and prognostic biomarker for early‑stage pancreatic ductal adenocarcinoma.Oncology reports · 2019Article
- Novel protein signatures suggest progression to muscular invasiveness in bladder cancer.PloS one · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystatin D (CST5) encodes an inhibitor of cysteine proteases of the cathepsin family and is directly induced by the vitamin D receptor (VDR). Interestingly, vitamin D3 exerts tumor suppressive effects in a variety of tumor types. In colorectal cancer (CRC) cells CST5 was shown to mediate mesenchymal-epithelial transition (MET). Interestingly, vitamin D3 was shown to exert tumor suppressive effects in a variety of tumor types, including colorectal cancer (CRC). We recently performed an integrated genomic and proteomic screen to identify targets of the p53 tumor suppressor in CRC cells. Thereby, we identified CST5 as a putative p53 target gene. Here, we validated and characterized CST5 as a direct p53 target gene. After activation of a conditional p53 allele, CST5 was upregulated on mRNA and protein levels. Treatment with nutlin-3a or etoposide induced CST5 in a p53-dependent manner. These regulations were direct, since ectopic and endogenous p53 occupied a conserved binding site in the CST5 promoter region. In addition, treatment with calcitriol, the active vitamin D3 metabolite, and simultaneous activation of p53 resulted in enhanced CST5 induction and increased repression of SNAIL, an epithelial-mesenchymal transition (EMT) inducing transcription factor. Furthermore, CST5 inactivation decreased p53-induced mesenchymal-epithelial transition (MET) as evidenced by decreased inhibition of SNAIL and of migration by p53. Furthermore, CST5 expression was directly repressed by SNAIL. In summary, these results imply CST5 as an important mediator of tumor suppression by p53 in colorectal cancer. In addition, they suggest that a combined treatment activating p53 and the vitamin D3 pathway may function via induction of CST5.
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