15 research outputs found

    Autophagy inhibitor sensitized pterostilbene and 3′-hydroxypterostilbene-induced apoptosis in COLO 205 cancer cells.

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    <p>Cells were pretreated with 25 µM CQ for 1 h before treatment with 50 µM of pterostilbene or 3′-hydroxypterostilbene for 24 h. (A) Cell viability was determined by MTT assay. (B, C) Sub-G1 cell population (%) was analyzed and quantification after PI staining followed by flow cytometry. Data were presented as mean ±SD of triplicate experiments. <sup>*</sup><i>P</i><0.05 and <sup>**</sup><i>P</i><0.01 indicates statistically significant difference from the pterostilbene-treated group.</p

    Bispecific antibodies (anti-mPEG/anti-HER2) for active tumor targeting of docetaxel (DTX)-loaded mPEGylated nanocarriers to enhance the chemotherapeutic efficacy of HER2-overexpressing tumors

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    <p>Anti-mPEG/anti-human epidermal growth factor receptor 2 (HER2) bispecific antibodies (BsAbs) non-covalently bound to a docetaxel (DTX)-loaded mPEGylated lecithin-stabilized micellar drug delivery system (L<i><sub>sb</sub></i>MDDs) were endowed with active targetability to improve the chemotherapeutic efficacy of DTX. DTX-loaded mPEGylated L<i><sub>sb</sub></i>MDDs formulations were prepared using lecithin/DSPE-PEG(2K or 5K) nanosuspensions to hydrate the thin film, and then they were subjected to ultrasonication. Two BsAbs (anti-mPEG/anti-DNS or anti-HER2) were simply mixed with the L<i><sub>sb</sub></i>MDDs to form BsAbs-L<i><sub>sb</sub></i>MDDs formulations, respectively, referred as the DNS-L<i><sub>sb</sub></i>MDDs and HER2-L<i><sub>sb</sub></i>MDDs. Results demonstrated that the physical characteristics of the BsAbs-L<i><sub>sb</sub></i>MDDs were similar to those of the plain L<i><sub>sb</sub></i>MDDs but more slowly released DTX than that from the L<i><sub>sb</sub></i>MDDs. Results also showed that the HER2-L<i><sub>sb</sub></i>MDDs suppressed the growth of HER2-expressing MCF-7/HER2 tumors, increasing the amount taken up <i>via</i> an endocytosis pathway leading to high drug accumulation and longer retention in the tumor. In conclusion, the BsAbs-L<i><sub>sb</sub></i>MDDs preserved the physical properties of the L<i><sub>sb</sub></i>MDDs and actively targeted tumors with a drug cargo to enhance drug accumulation in tumors leading to greater antitumor activity against antigen-positive tumors.</p

    3′-Hydroxypterostilbene down-regulated mTOR, PI3K/Akt and MAPKs signaling in COLO 205 cancer cells.

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    <p>COLO 205 cells were treated with 50 µM 3′-hydroxypterostilbene at different times. Cell lyates were prepared and the protein levels of (A) p-mTOR, p-P70S6K, (B) p-PI3K, p-Akt and (C) p-ERK1/2, p-JNK1/2, p-p38 were analyzed by Western blotting analysis. All analyses were representative of at least three independent experiments. The values under each lane indicate relative density of the band normalized to β-actin using a densitometer.</p

    Pterostilbene and 3′-hydroxypterostilbene reduced the growth of COLO 205 xenografts in nude mice.

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    <p>Experimental treatment protocol as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111814#s2" target="_blank">Materials and Methods</a>. Mice bearing COLO 205 xenografts were <i>i.p.</i> injection with pterostilbene or 3′-hydroxypterostilbene for 15 days where control group was received corn oil. (A) Photograph of xenograft tumors developed in each group is shown at the end of day15. (B) Average tumor volumes were recorded during the treatment and (C) average tumor weights were measured at the end of experiment. Six samples were analyzed in each group, and values represent the mean ±SD. <sup>*</sup><i>P</i><0.05 and <sup>**</sup><i>P</i><0.01, compared with control group. <sup>#</sup><i>P</i><0.05, compared with pterostilbene-treated group. (D) Total proteins of xenograft tumors in each group were extracted for western blot analysis. COX-2, MMP-9, VEGF, PCNA, cyclin D1 protein expression and cleaved caspase-3 were detected by using specific antibodies. Similar results were obtained in three independent experiments.</p

    Pterostilbene and 3′-hydroxypterostilbene induced apoptosis in COLO205 cancer cells.

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    <p>Cells were treated with various concentrations (5, 10, 25 and 50 µM) of pterostilbene or 3′-hydroxypterostilbene for 24 h. (A) Determination of sub-G1 cells in COLO 205 cells by flow cytometry after PI staining as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111814#s2" target="_blank">Materials and Methods</a>. (B, C) After treatment, total cell lysates were prepared from COLO 205 cells and the cleavage of PARP, DFF-45, pro-caspase 8 and pro-caspase 9 were analyzed by Western blotting. (D) Kinetics of caspase activation in COLO 205 cells. Cells were treated with 25 and 50 µM of pterostilbene or 3′-hydroxypterostilbene for 24 h. Caspase activities were analyzed as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111814#s2" target="_blank">Materials and Methods</a>. (E) Cells were treated with 50 µM of pterostilbene or 3′-hydroxypterostilbene for 15 min. Mitochondrial membrane potential and ROS production were stained with DiOC6 (40 nM) and DCFH-DA (20 µM) and measured by flow cytometry. The values are expressed as means ±SE of triplicate tests. *<i>P</i><0.05 indicates statistically significant difference from the pterostilbene-treated group.</p

    Autophagy induction by pterostilbene and 3′-hydroxypterostilbene in COLO 205 cancer cells.

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    <p>Cells were treated with 50 µM pterostilbene or 3′-hydroxypterostilbene for 24 h and stained with acridine orange. (A) Green and red fluorescence in acridine orange-stained cells were observed under fluorescence microscope. (B, C) Detection and quantification of autophagy in COLO 205 cells. Cells were treated with 25 and 50 µM of pterostilbene or 3′-hydroxypterostilbene for 24 h and stained with acridine orange. The measurement of green and red fluorescence in acridine orange-stained cells was performed using flow cytometry. (D) Cell lysates were prepared after 24 h treatment and the protein expression of LC3 I/II were analyzed by Western blotting. Data were presented as mean ±SD of triplicate experiments. *<i>P</i><0.05 indicates statistically significant difference from the pterostilbene-treated group.</p

    Effects of pterostilbene and 3′-hydroxypterostilbene administration on the body weight and organ weight in a COLO 205 xenograft model<sup>a</sup>.

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    a<p>COLO 205 cells were injected into 3–4 week old BALB/c nude mice (5×10<sup>6</sup> cells per mouse). After tumors grew to about 100–200 mm<sup>3</sup>, mice were <i>i.p.</i> treated with pterostilbene or 3′-hydroxypterostilbene for 15 days. All mice of each group were sacrificed by CO<sub>2</sub> asphyxiation at the end of experiment. Comparisons were analyzed using ANOVA followed by Fisher's least significant difference test.</p><p>Effects of pterostilbene and 3′-hydroxypterostilbene administration on the body weight and organ weight in a COLO 205 xenograft model<sup><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111814#nt102" target="_blank">a</a></sup>.</p

    The incidence and lung tumor multiplicity of lung tumor formation in A/J mice treated with NNK, NNK combined with TCDD, E2, or both.

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    <p>* Significantly higher (<i>p</i><0.05) compared to Sham, control groups.</p>†<p>Significantly higher (<i>p</i><0.05) compared to Sham, NNK groups.</p>#<p>Significantly higher (<i>p</i><0.05) compared to OVX, NNK groups.</p>‡<p>Significantly higher (<i>p</i><0.05) compared to OVX, NNK+TCDD groups.</p>§<p>Significantly higher (<i>p</i><0.05) compared to OVX, NNK+E2 groups.</p><p>Tumor incidences are given as the number of animals with tumors/total number of animals at risk (%). Tumor multiplicity is the average tumor number on tumor-bearing mice. Data of lung tumor multiplicity are given as the mean ± SEM.</p><p>*significantly higher (<i>p</i><0.05) compared to Sham, Control groups,</p>#<p>significantly higher (p<0.05) compared to OVX, NNK groups,</p>†<p>significantly higher (<i>p</i><0.05) compared to Sham, NNK groups,</p>‡<p>significantly higher (<i>p</i><0.05) compared to OVX, NNK+TCDD groups,</p>§<p>significantly higher (<i>p</i><0.05) compared to OVX, NNK+E2 groups.</p

    Examination of lung tumors on A/J mice.

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    <p>Tumor pathology of lung tumors in A/J mice treated with NNK for 24 weeks. (a) Images of the lung surface indicate that NNK-treated mice lungs presented with numerous visible lesions (black circles) and (b) the histological characteristics of mouse lungs stained with H&E from control and NNK treatment groups. Arrows indicate the adenocarcinoma in the lungs (magnification, ×100).</p
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