Altered cell cycle response of drug-resistant lung carcinoma cells to doxorubicin

O’Loughlin, Colette; Heenan, Mary; Coyle, Shirley; Clynes, Martin

doi:10.1016/s0959-8049(00)00071-x

Cited by 26 publications

(18 citation statements)

References 22 publications

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“…Actually, in cell cycle analysis according to doxorubicin concentration, transient G 2 /M arrest occurred up to 2 mg/mL, and G 1 arrest progressed with concentrations of 3 mg/mL or higher. Our data are concordant with the demonstration of O'Loughlin et al (29) in which transient G 2 /M arrest and subsequent progression into G 1 occurred dependent on doxorubicin exposure time in drug-resistant carcinoma cells.…”

Section: Discussionsupporting

confidence: 93%

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

Kim

Kang

Chung

et al. 2007

Journal of Nuclear Medicine

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We investigated the effect of doxorubicin on transgene expression and evaluated the mechanism of enhanced transgene expression by doxorubicin in transfected human anaplastic thyroid cancer cells (ARO cells). Methods: ARO cells were transfected with plasmid vectors or adenoviral vectors expressing human sodium/iodide symporter (hNIS) or luciferase (Luc) under the control of cytomegalovirus (CMV) promoter. After treating transfected and control ARO cells with doxorubicin, iodide uptake assay and luciferase assay were performed. Reversedphase polymerase chain reaction analysis for hNIS and Western blot analysis for IkB protein were executed. Electrophoretic mobility-shift assay (EMSA) was performed to evaluate nuclear factor-kB (NF-kB) binding activity induced by doxorubicin. Scintigraphic and bioluminescent images were acquired and quantitated before and after doxorubicin in a tumor-bearing mouse model. Results: Radioiodide uptake in ARO cells transfected with the NIS gene under the CMV promoter was remarkably enhanced by doxorubicin, and this corresponded to a significant increase in NIS messenger RNA. In addition, luciferase gene upregulation by doxorubicin was also observed in luciferase gene transfected ARO cells. These results were verified by in vivo imaging in a tumorbearing mouse model. Moreover, transgene expressional enhancement by doxorubicin was observed after transfecting ARO cells with adenoviral vector or plasmid vector, when transgenes were under the control of a CMV promoter. In addition, NF-kB, activated by doxorubicin, induced transgene transcription under the control of the CMV promoter, which possesses an NF-kB binding site. Conclusion: These findings indicate that doxorubicin enhances transgene expression under the control of the CMV promoter and that doxorubicin might be used as an adjuvant to radioiodine therapy by NIS gene transfer in anaplastic thyroid carcinoma.

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Section: Discussionsupporting

confidence: 93%

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

Kim

Kang

Chung

et al. 2007

Journal of Nuclear Medicine

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“…It has been shown that phosphorylation of histone H3 at Ser-10 (H3S10P) (33) and dephosphorylation of Cdc2 at Tyr-15 (Cdc2Y15P) (31,34) are indicative of transition between G 2 -and M-phases. As shown in Fig.…”

Section: Hxdv Exhibits Anti-proliferative Activity Against Tumor Cellmentioning

confidence: 99%

A G-quadruplex Stabilizer Induces M-phase Cell Cycle Arrest

Tsai¹,

Qi²,

Lin³

et al. 2009

Journal of Biological Chemistry

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G-quadruplex stabilizers such as telomestatin and HXDV bind with exquisite specificity to G-quadruplexes, but not to triplex, duplex, or single-stranded DNAs. Studies have suggested that the antiproliferative and possibly anti-tumor activities of these compounds are linked to their inhibitory effect on telomerase and/or telomere function. In the current studies, we show that HXDV, a synthetic analog of telomestatin, exhibits antiproliferative activity against both telomerase-positive and -negative cells and induces robust apoptosis within 16 h of treatment, suggesting a mode of action independent of telomerase. HXDV was also shown to inhibit cell cycle progression causing M-phase cell cycle arrest, as evidenced by accumulation of cells with 4 N DNA content, increased mitotic index, separated centrosomes, elevated histone H3 phosphorylation at Ser-10 (an M-phase marker), and defective chromosome alignment and spindle fiber assembly (revealed by time-lapse microscopy). The M-phase arrest caused by HXDV paralleled with reduction in the expression level of the major M-phase checkpoint regulator Aurora A. All these cellular effects appear to depend on the G-quadruplex binding activity of HXDV as its non-G-quadruplex binding analog, TXTLeu, is completely devoid of all these effects. In the aggregate, our results suggest that HXDV, which exhibits anti-proliferative and apoptotic activities, is also a novel M-phase blocker, with a mode of action dependent on its G-quadruplex binding activity.

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“…The cell lines DLKP (37), DLKP-A (39) and DLKP-A5F (40) were cultured in minimal essential medium/Ham's F12 (1:1, v/v) supplemented with 5% fetal calf serum and 2 mM L-glutamine. A549 was cultured in Dulbecco's modified Eagle's medium/Hams F12 (1:1, v/v) supplemented with 5% fetal calf serum.…”

Section: Experimental Cell Preparationmentioning

confidence: 99%

Metabolomic studies of human lung carcinoma cell lines using in vitro¹H NMR of whole cells and cellular extracts

et al. 2008

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We report principal component analysis (PCA) of (1)H NMR spectra recorded for a group of human lung carcinoma cell lines in culture and (1)H NMR analysis of extracts from the same samples. The samples studied were cells of lung tumour origin with different chemotherapy drug resistance patterns. For whole cells, it was found that the statistically significant causes of spectral variation were an increase in the choline and a decrease in the methylene mobile lipid (1)H resonance intensities, which correlate with our knowledge of the level of resistance displayed by the different cells. Similarly, in the (1)H NMR spectra of the aqueous and lipophilic extracts, significant quantitative differences in the metabolite distributions were apparent, which are consistent with the PCA results.

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Altered cell cycle response of drug-resistant lung carcinoma cells to doxorubicin

Cited by 26 publications

References 22 publications

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

A G-quadruplex Stabilizer Induces M-phase Cell Cycle Arrest

Metabolomic studies of human lung carcinoma cell lines using in vitro¹H NMR of whole cells and cellular extracts

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Altered cell cycle response of drug-resistant lung carcinoma cells to doxorubicin

Cited by 26 publications

References 22 publications

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

Doxorubicin Enhances the Expression of Transgene Under Control of the CMV Promoter in Anaplastic Thyroid Carcinoma Cells

A G-quadruplex Stabilizer Induces M-phase Cell Cycle Arrest

Metabolomic studies of human lung carcinoma cell lines using in vitro1H NMR of whole cells and cellular extracts

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Metabolomic studies of human lung carcinoma cell lines using in vitro¹H NMR of whole cells and cellular extracts