ArticleThe American journal of pathology2004
Expression of myopodin induces suppression of tumor growth and metastasis.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
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- Synaptopodin-2: a potential tumor suppressor.Cancer cell international · 2023Review
- Vitamin C Inhibits Triple-Negative Breast Cancer Metastasis by Affecting the Expression of YAP1 and Synaptopodin 2.Nutrients · 2019Article
- The role of zyxin in regulation of malignancies.Heliyon · 2018Review
- MAN2A1-FER Fusion Gene Is Expressed by Human Liver and Other Tumor Types and Has Oncogenic Activity in Mice.Gastroenterology · 2017Article
- Oncogenic activity of amplified miniature chromosome maintenance 8 in human malignancies.Oncogene · 2017Article
- Myopodin methylation is a prognostic biomarker and predicts antiangiogenic response in advanced kidney cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Prognostic Significance of Promoter Hypermethylation and Diminished Gene Expression of SYNPO2 in Melanoma.The Journal of investigative dermatology · 2015Article
- Oncogenic Activity of miR-650 in Prostate Cancer Is Mediated by Suppression of CSR1 Expression.The American journal of pathology · 2015Article
- Article
- Integrin α7 binds tissue inhibitor of metalloproteinase 3 to suppress growth of prostate cancer cells.The American journal of pathology · 2013Article
- Chaperone-assisted proteostasis is essential for mechanotransduction in mammalian cells.Communicative & integrative biology · 2013Article
- Metallothionein 1 h tumour suppressor activity in prostate cancer is mediated by euchromatin methyltransferase 1.The Journal of pathology · 2013Article
- Interaction of MCM7 and RACK1 for activation of MCM7 and cell growth.The American journal of pathology · 2013Article
- Myopodin is an F-actin bundling protein with multiple independent actin-binding regions.Journal of muscle research and cell motility · 2013Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Myopodin was previously reported as a gene that was frequently deleted in prostate cancer. This gene shares significant homology with a cell shape-regulating gene, synaptopodin. Myopodin was shown to bind actin and to induce actin bundling when cells were stimulated. To clarify the functional role of myopodin in prostate cancer, several assays were performed to evaluate the tumor suppression activity of myopodin. Our results indicate that myopodin inhibits tumor growth and invasion both in vitro and in vivo. The activity of tumor suppression of myopodin is located at the C-terminus region. To further evaluate the role of myopodin in suppressing the invasiveness of prostate cancer, an expression analysis of myopodin protein was performed in prostate tissues. The results indicate that down-regulation of myopodin expression occurs mostly in invasive stages of prostate cancer, implying a potential invasion suppression role for myopodin in prostate cancer. In addition, hemizygous deletion and down-regulation of myopodin expression occur in three aggressive prostate cancer cell lines. All these results support the hypothesis that myopodin functions as a tumor suppressor gene to limit the growth and to inhibit the metastasis of cancer cells.
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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.