ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
Synergistic induction of apoptosis and chemosensitization of human colorectal cancer cells by histone deacetylase inhibitor, scriptaid, and proteasome inhibitors: potential mechanisms of action.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses 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.
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
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- Association between IRS-1 Gly972Arg polymorphism and colorectal cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Association between IL-4 -589C>T polymorphism and colorectal cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- The MOGA multi-modal framework based on graph augmentation networks for drug response prediction.iScience · 2026Article
- Patient-Derived Organoid Serves as a Platform for Personalized Chemotherapy in Advanced Colorectal Cancer Patients.Frontiers in oncology · 2022Article
- Passiflora caerulea L. fruit extract and its metabolites ameliorate epileptic seizure, cognitive deficit and oxidative stress in pilocarpine-induced epileptic mice.Metabolic brain disease · 2020Article
- Article
- Review
- Prolonged proteasome inhibition cyclically upregulates Oct3/4 and Nanog gene expression, but reduces induced pluripotent stem cell colony formation.Cellular reprogramming · 2015Article
- Overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Association between interleukin-4 gene intron 3 VNTR polymorphism and cancer risk.Cancer cell international · 2014Article
- NF-κB in colorectal cancer.Journal of molecular medicine (Berlin, Germany) · 2013Review
- The complexity of NF-κB signaling in inflammation and cancer.Molecular cancer · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase inhibitors (HDACIs) exhibit modest results as single agents in preclinical and clinical studies against solid tumors; they often fall short and activate nuclear factor kappa-B (NFκB). Co-administration of HDACI with proteasome inhibitors (PIs), which interrupt NFκB pathways, may enhance HDACI-lethality. The goal of this study was to determine whether PIs could potentiate HDACI, scriptaid (SCP)-mediated lethality, to unravel the associated mechanisms and to assess the effects of the combined inhibition of HDAC and proteasome on chemotherapy response in human colorectal cancer cells. Cancer cells were exposed to agents alone or in combination; cell growth inhibition was determined by MTT and colony formation assays. HDAC-, proteasome-, NFκB-activities, and reactive oxygen species (ROS) were quantified. Induction of apoptosis and cell cycle alterations were monitored by flow cytometry. Expression of cell cycle/apoptosis and cytoprotective/stress-related genes was determined by real-time qRT-PCR and EIA, respectively. Potentiation of cancer cell sensitivity to chemotherapies by SCP/PIs was also evaluated. SCP and PIs: MG132, PI-1, or epoxomicin interact synergistically to potently inhibit cancer cell growth, alter cell cycle, induce apoptosis, reduce NFκB activity, and increase ROS generation. These events are associated with multiple perturbations in the expression of cell cycle, apoptosis, cytoprotective, and stress-related genes. Co-administration of SCP and PIs strikingly increases the chemosensitivity of cancer cells (122-2 × 10(5)-fold) in a drug and SCP/PIs-dependent manner. This combination regimen markedly reduced the doses of chemotherapies with potent anticancer effects and less toxicity. A strategy combining HDAC/proteasome inhibition with chemotherapies warrants further investigation in colorectal cancer.
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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.