ArticleJournal of cancer research and clinical oncology2012
Survivin inhibition by an interacting recombinant peptide, derived from the human ferritin heavy chain, impedes tumor cell growth.
Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
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
10 citing papers in PubMed, 21 citations in OpenAlex.
- Ferritin as an Effective Prognostic Factor and Potential Cancer Biomarker.Current issues in molecular biology · 2025Review
- Review
- Ferritins in Kidney Disease.Seminars in nephrology · 2020Review
- Dysregulation of the intrinsic apoptotic pathway mediates megakaryocytic hyperplasia in myeloproliferative neoplasms.Journal of clinical pathology · 2016Article
- Association of survivin splice variants with prognosis and treatment of breast cancer.World journal of clinical oncology · 2014Review
- Oncoapoptotic markers in oral cancer: prognostics and therapeutic perspective.Molecular diagnosis & therapy · 2014Review
- Targeting survivin in cancer: novel drug development approaches.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2014Review
- Targeting oncogenic ALK and MET: a promising therapeutic strategy for glioblastoma.Metabolic brain disease · 2013Review
- Targeting malignant mitochondria with therapeutic peptides.Therapeutic delivery · 2012Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProteins involved in the aberrant regulation of signaling pathways and their downstream effectors are promising targets for cancer therapy. Survivin is an anti-apoptotic and cell cycle-promoting protein, which is consistently overexpressed in cancer cells. In normal cells, its expression is tightly controlled by signaling pathways and their associated transcriptional activators and repressors. In cancer cells, its expression is enhanced as a consequence of oncogenic signaling. We investigated the potential of a novel, peptide-based survivin inhibitor in breast cancer (SK-BR-3, MDA-MB-468) and glioblastoma (Tu9648) cells. These cells express high levels of survivin. MATERIALS AND
methodsWe downregulated survivin expression in tumor cells with a lentiviral gene transfer vector encoding a specific shRNA and a recombinant fusion protein, rSip, comprising the FTH1-derived survivin interaction domain, the human thioredoxin and a protein transduction domain.
resultsDownregulation of survivin expression decreased the growth and viability of tumor cells in culture and reduced growth of the cancer cells upon transplantation into immunodeficient mice. rSip selectively targets the anti-apoptotic function of survivin and causes tumor cell death. Non-transformed NIH/3T3 and MCF10A cells remain unaffected.
conclusionsrSip provides a lead structure for the development of drugs targeting the tumor cell "addiction protein" survivin.
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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.