dehydroxymethylepoxyquinomicin and Carcinoma--Squamous-Cell

dehydroxymethylepoxyquinomicin has been researched along with Carcinoma--Squamous-Cell* in 2 studies

Other Studies

2 other study(ies) available for dehydroxymethylepoxyquinomicin and Carcinoma--Squamous-Cell

ArticleYear
Anti-tumor activity of dehydroxymethylepoxyquinomicin against human oral squamous cell carcinoma cell lines in vitro and in vivo.
    Oral oncology, 2011, Volume: 47, Issue:5

    Several reports have indicated that nuclear factor-kappa B (NF-κB) is constitutively activated in a variety of cancer cells including human oral squamous carcinoma cells, and play a key role in their growth and survival. Recent studies report that NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), inhibits proliferation and induces apoptosis in prostate cancer cell lines. However this anti-tumor effects are still unknown in end human oral squamous carcinoma cells. In the present study, we investigated the effects of DHMEQ on oral squamous carcinoma cell (OSCC) lines in vitro and in vivo. Human OSCC cell lines (HSC-3, SAS) were treated with DHMEQ and examined for cell viability by MTT assay, cell cycle distribution by flow-cytometry, apoptosis by TUNEL assay, and protein expression by western blotting, respectively. In vivo activities were also investigated in a mouse xenograft model. DHMEQ inhibited growth of two OSCC cell lines in a dose-dependent manner measured by MTT assay. A flow cytometric analysis demonstrated that treatment with DHMEQ induced accumulation in sub-G1 phase. TUNEL assay showed that DHMEQ induced DNA fragmentation. Protein expression by western blotting analysis revealed that DHMEQ induced nuclear down regulation of Survivin, cIAP-1, and cIAP-2. In nude mice, DHMEQ inhibited growth of OSCC without major toxic side effects. The present results demonstrated that administration of DHMEQ is suggested to be a novel anti-tumor approach to the treatment of OSCC.

    Topics: Animals; Antineoplastic Agents; Benzamides; Carcinoma, Squamous Cell; Cell Cycle; Cell Line, Tumor; Cyclohexanones; Dose-Response Relationship, Drug; Flow Cytometry; Humans; Inhibitor of Apoptosis Proteins; Mice; Mouth Neoplasms; NF-kappa B; Reverse Transcriptase Polymerase Chain Reaction; Tumor Cells, Cultured

2011
Effects of a novel NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on growth, apoptosis, gene expression, and chemosensitivity in head and neck squamous cell carcinoma cell lines.
    Head & neck, 2006, Volume: 28, Issue:2

    Recent studies provide evidence that the constitutive activation of nuclear factor-kappa B, NF-kappaB plays a critical role in enhancing the growth of several types of malignancies, including head and neck squamous cell carcinoma (HNSCC).. In this study, we examined the effects of a newly synthesized NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on growth, induction of apoptosis, gene expression, and chemosensitivity in two HNSCC cell lines (YCU-H891 and KB), which expressed high levels of nuclear NF-kappaB protein.. DHMEQ showed strong growth inhibitory effects on these two cell lines, with a 50% cell growth inhibition (IC50) concentration of approximately 20 microg/mL. These growth inhibitory effects were associated with inhibition of the NF-kappaB activity. Treatment with DHMEQ induced apoptosis in a dose-dependent manner accounting, at least in part, for the growth inhibition by DHMEQ. DHMEQ strongly inhibited cyclin D1 and vascular endothelial growth factor (VEGF) promoter activity and decreased the levels of cyclin D1 protein and VEGF mRNA in KB cells. In addition, low concentrations of DHMEQ (1.0 or 5.0 microg/mL) synergistically enhanced the cellular sensitivity of YCU-H and KB cells to cisplatin, which is a key chemotherapeutic agent in the treatment of HNSCC.. These results suggest that DHMEQ may be effective when used alone or in combination with other agents in the treatment of HNSCC.

    Topics: Apoptosis; Benzamides; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Proliferation; Cyclin D1; Cyclohexanones; Gene Expression; Head and Neck Neoplasms; Humans; NF-kappa B; Vascular Endothelial Growth Factor A

2006