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Survivin and YM155: how faithful is the liaison?
Anke Rauch1, Dorle Hennig1, Claudia Schäfer1
1Center for Molecular Biomedicine, Institute for Biochemistry and Biophysics, Department of Biochemistry, Friedrich Schiller University of Jena, Hans-Knöll-Straße 2, 07745 Jena, Germany.
Abstract:
Survivin belongs to the family of apoptosis inhibitors (IAPs), which antagonizes the induction of cell death. Dysregulated expression of IAPs is frequently observed in cancers, and the high levels of survivin in tumors compared to normal adult tissues make it an attractive target for pharmacological interventions. The small imidazolium-based compound YM155 has recently been reported to block the expression of survivin via inhibition of the survivin promoter. Recent data, however, question that this is the sole and main effect of this drug, which is already being tested in ongoing clinical studies. Here, we critically review the current data on YM155 and other new experimental agents supposed to antagonize survivin. We summarize how cells from various tumor entities and with differential expression of the tumor suppressor p53 respond to this agent in vitro and as murine xenografts. Additionally, we recapitulate clinical trials conducted with YM155. Our article further considers the potency of YM155 in combination with other anti-cancer agents and epigenetic modulators. We also assess state-of-the-art data on the sometimes very promiscuous molecular mechanisms affected by YM155 in cancer cells.
Insights
YM155 is an experimental drug targeting survivin, a protein involved in cancer cell survival. This review examines its effectiveness, mechanisms, and clinical trials, exploring its potential in combination therapies for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Survivin, an apoptosis inhibitor, is upregulated in many cancers, making it a therapeutic target.
- YM155 is an experimental drug designed to inhibit survivin expression.
- Recent findings suggest YM155 may have additional mechanisms beyond survivin promoter inhibition.
Purpose of the Study:
- To critically review current data on YM155 and other survivin-targeting agents.
- To summarize the in vitro and in vivo responses of various tumor cells to YM155.
- To assess the clinical trial data, combination therapy potential, and molecular mechanisms of YM155.
Main Methods:
- Literature review of preclinical and clinical studies on YM155.
- Analysis of cellular responses in various tumor types and p53 expression levels.
- Evaluation of YM155 in combination with other anti-cancer agents and epigenetic modulators.
Main Results:
- YM155's efficacy varies across tumor types and is influenced by p53 status.
- Clinical trials provide insights into YM155's safety and preliminary efficacy.
- YM155 exhibits complex and potentially promiscuous molecular interactions in cancer cells.
Conclusions:
- YM155 shows promise as a survivin-targeting agent, but its precise mechanisms require further elucidation.
- Combination therapies involving YM155 may enhance anti-cancer effects.
- Understanding YM155's multifaceted actions is crucial for optimizing its clinical application.
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