ArticleMolecular cancer therapeutics2006
The mechanism of methylselenocysteine and docetaxel synergistic activity in prostate cancer cells.
Article in Molecular cancer therapeutics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
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- DIGRE: Drug-Induced Genomic Residual Effect Model for Successful Prediction of Multidrug Effects.CPT: pharmacometrics & systems pharmacology · 2015Article
- Simultaneous Dual Selective Targeted Delivery of Two Covalent Gemcitabine Immunochemotherapeutics and Complementary Anti-Neoplastic Potency of [Se]-Methylselenocysteine.Journal of cancer therapy · 2015Article
- Comparison of oxidized porous silicon with bare porous silicon as a photothermal agent for cancer cell destruction based on in vitro cell test results.Lasers in medical science · 2012Article
- Prostate-derived Ets transcription factor (PDEF) is a potential prognostic marker in patients with prostate cancer.The Prostate · 2011Article
- Porous silicon nanoparticles for cancer photothermotherapy.Nanoscale research letters · 2011Article
- Targeting the oncogenic protein beta-catenin to enhance chemotherapy outcome against solid human cancers.Molecular cancer · 2010Article
- Se-methylselenocysteine sensitizes hypoxic tumor cells to irinotecan by targeting hypoxia-inducible factor 1alpha.Cancer chemotherapy and pharmacology · 2010Article
- Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition.BMC cancer · 2010Article
- Generation of a novel transgenic mouse model for bioluminescent monitoring of survivin gene activity in vivo at various pathophysiological processes: survivin expression overlaps with stem cell markers.The American journal of pathology · 2010Article
- Downregulation of cystine transporter xc by irinotecan in human head and neck cancer FaDu xenografts.Chemotherapy · 2010Article
- Enhancing effectiveness of the MDR-sensitive compound T138067 using advanced treatment with negative modulators of the drug-resistant protein survivin.American journal of translational research · 2009Article
- Mechanisms of drug combinations: interaction and network perspectives.Nature reviews. Drug discovery · 2009Review
- Chemotherapeutic sensitization by endoplasmic reticulum stress: increasing the efficacy of taxane against prostate cancer.Cancer biology & therapy · 2009Article
- Prostate-derived Ets transcription factor as a favorable prognostic marker in ovarian cancer patients.International journal of cancer · 2008Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The study was designed to evaluate the combination treatment of methylselenocysteine (MSeC) and docetaxel and to delineate the underlying mechanism associated with observed in vitro synergy between MSeC and docetaxel in prostate cancer cells. Cells were treated with different concentrations and schedules (concurrent or sequential) of MSeC and docetaxel alone or in combination. Cell growth/death was assessed with sulforhodamine B assay, trypan blue assay, and time-lapse video. Loewe synergism/antagonism model was used to determine whether the combination effect was additive, synergistic, or antagonistic. Apoptosis and caspase-3 activity were evaluated with cell death ELISA assay and caspase activity assay, respectively. Synergy between MSeC and docetaxel was further assessed in the presence and absence of z-VAD-fmk, a pan-caspase inhibitor. Effect of MSeC and docetaxel alone or in combination on the cellular expression of the antiapoptotic protein survivin was measured with Western blot analyses. Pretreatment with MSeC was crucial to enhance docetaxel antitumor activity. The enhanced antitumor activity of the sequential combination treatment of MSeC and docetaxel (MSeC/docetaxel) was highly synergistic. Apoptosis increased after MSeC/docetaxel, compared with each drug alone or concurrent treatment. Pretreatment with z-VAD-fmk converted the synergy into antagonism, suggesting that the synergy is caspase-dependent apoptosis. The survivin level was down-regulated following MSeC/docetaxel treatment when compared with each drug alone. In conclusion, pretreatment with MSeC was essential to markedly sensitize cells to docetaxel. The synergy between MSeC and docetaxel in C2G prostate cancer cells is associated with increased level of caspase-dependent apoptosis and decreased level of 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.