Echinomycin and a novel analogue induce apoptosis of HT-29 cells via the activation of MAP kinases pathway

Park, Ju Youn; Park, Su Jung; Shim, Kwang Yong; Lee, Kyu-Jae; Kim, Yun Bong; Kim, Yong Hae; Kim, Soo Kie

doi:10.1016/j.phrs.2004.01.005

Cited by 15 publications

(11 citation statements)

References 30 publications

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“…A) is a quinoxaline antibiotic that also binds to DNA duplexes by bis‐intercalation and interferes with both replication and transcription . These types of compounds have great potential as anticancer agents . Therefore, the investigation of the interaction between echinomycin and DNA will be very helpful for drug optimization and novel design.…”

Section: Intercalating Into Dnamentioning

confidence: 99%

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Structure-Based DNA-Targeting Strategies with Small Molecule Ligands for Drug Discovery

2013

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Nucleic acids are the molecular targets of many clinical anticancer drugs. However, compared with proteins, nucleic acids have traditionally attracted much less attention as drug targets in structure-based drug design, partially because limited structural information of nucleic acids complexed with potential drugs is available. Over the past several years, enormous progresses in nucleic acid crystallization, heavy-atom derivatization, phasing, and structural biology have been made. Many complicated nucleic acid structures have been determined, providing new insights into the molecular functions and interactions of nucleic acids, especially DNAs complexed with small molecule ligands. Thus, opportunities have been created to further discover nucleic acid-targeting drugs for disease treatments. This review focuses on the structure studies of DNAs complexed with small molecule ligands for discovering lead compounds, drug candidates, and/or therapeutics.

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Section: Intercalating Into Dnamentioning

confidence: 99%

“…132 These types of compounds have great potential as anticancer agents. 133 Therefore, the investigation of the interaction between echinomycin and DNA will be very helpful for drug optimization and novel design. Several NMR structure studies have been reported for echinomycin-bound DNA r SHENG, GAN AND HUANG complexes.…”

Section: Intercalating Into Dnamentioning

confidence: 99%

Structure-Based DNA-Targeting Strategies with Small Molecule Ligands for Drug Discovery

2013

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“…Echinomycin-initiated apoptosis in HT-29 cell occurs via mitochondrial dependent MAP kinase-caspase pathway (Park et al, 2004(Park et al, , 2008. In the light of convergeable, downstream signaling, so echinomycin-initiated apoptosis might be NF-kB-dependent.…”

Section: Discussionmentioning

confidence: 99%

NF‐κB‐dependency and consequent regulation of IL‐8 in echinomycin‐induced apoptosis of HT‐29 colon cancer cells

Park

Chang

Bae

et al. 2008

Cell Biology International

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The present study was to see whether echinomycin-induced apoptosis would be NF-kappaB-dependent and if so, whether echinomycin would activate or inhibit NF-kappaB as well as resultant chemokine IL-8 expression. In HT-29 cells echinomycin activated NF-kappaB in time-dependent manner. EMSA in the presence of antibodies specific for p50 and p65 subunits indicated that echinomycin-induces the translocation of p50-p65 heterodimeric subunits of NF-kappaB. Levels of IkappaB were detected at initial echinomycin treatment and thereafter decreased, faintly seen after a 6h treatment. In contrast p-IkappaB levels were clearly detected throughout 6-24h of echinomycin treatment, albeit initially fainted. To clarify the role of NF-kappaB on IL-8 expression in echinomycin-mediated apoptosis of HT-29 cells, ELISA plus RT-PCR clearly showed that IL-8 production is inducible by echinomycin treatment. Using a specific inhibitor, IL-8 regulation at echinomycin treatment in HT-29 cells occurred via both caspase-3 and NF-kappaB-dependent signal pathway. To confirm whether two different pathways (NF-kappaB and caspase) would be coupled, only NF-kappaB inhibitor (PDTC) and caspase-3 specific inhibitor (Z-DEVD-FMK) together significantly attenuated echinomycin-initiated apoptosis of HT-29 cells, pretreatment of HT-29 cells with PDTC rarely affected echinomycin-induced caspase-3 activation. So echinomycin-induced apoptosis in HT-29 cells occurs via NF-kappaB activation independent of caspase-3 activation modulating the resultant-linked key chemokine IL-8 expression and echinomycin-induced apoptosis is NF-kappaB-dependant and directly related to NF-kappaB activation, consequently regulating IL-8 expression.

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“…Kim et al showed the increased stiffness of highly metastatic human breast cancer cells after the activation of β-adrenergic signaling by βAR agonists, as well as an increased invasiveness of these cells in vitro [6]. These results were discussed in relation to the underlying mechanical mechanism of action in cancer cells [54]. (Figure 4).…”

Section: Effects Of the Anticancer Compound Echinomycin On The Viscoementioning

confidence: 96%

Examination of the relationship between viscoelastic properties and the invasion of ovarian cancer cells by atomic force microscopy

Chen¹,

Zeng²,

Ruan³

et al. 2020

Beilstein J. Nanotechnol.

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The mechanical properties of cells could serve as an indicator for disease progression and early cancer diagnosis. This study utilized atomic force microscopy (AFM) to measure the viscoelastic properties of ovarian cancer cells and then examined the association with the invasion of ovarian cancer at the level of living single cells. Elasticity and viscosity of the ovarian cancer cells OVCAR-3 and HO-8910 are significantly lower than those of the human ovarian surface epithelial cell (HOSEpiC) control. Further examination found a dramatic increase of migration/invasion and an obvious decease of microfilament density in OVCAR-3 and HO-8910 cells. Also, there was a significant relationship between viscoelastic and biological properties among these cells. In addition, the elasticity was significantly increased in OVCAR-3 and HO-8910 cells after the treatment with the anticancer compound echinomycin (Ech), while no obvious change was found in HOSEpiC cells after Ech treatment. Interestingly, Ech seemed to have no effect on the viscosity of the cells. Ech significantly inhibited the migration/invasion and significantly increased the microfilament density in OVCAR-3 and HO-8910 cells, which was significantly related with the elasticity of the cells. An increase of elasticity and a decrease of invasion were found in OVCAR-3 and HO-8910 cells after Ech treatment. Together, this study clearly demonstrated the association of viscoelastic properties with the invasion of ovarian cancer cells and shed a light on the biomechanical changes for early diagnosis of tumor transformation and progression at single-cell level.

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Echinomycin and a novel analogue induce apoptosis of HT-29 cells via the activation of MAP kinases pathway

Cited by 15 publications

References 30 publications

Structure-Based DNA-Targeting Strategies with Small Molecule Ligands for Drug Discovery

Structure-Based DNA-Targeting Strategies with Small Molecule Ligands for Drug Discovery

NF‐κB‐dependency and consequent regulation of IL‐8 in echinomycin‐induced apoptosis of HT‐29 colon cancer cells

Examination of the relationship between viscoelastic properties and the invasion of ovarian cancer cells by atomic force microscopy

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