Pancreatic cancer xenograft mouse model,
Received Mar 9; Accepted Apr 8.
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Copyright © Chi-Ming Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Associated Data Supplementary Materials S1. The error bars indicate standard error of the average.
Significance was determined pancreatic cancer xenograft mouse model the Student t-test. All animals were humanely sacrificed after 4 weeks of monitoring due to the excessive tumor burden. However, radiation-induced tumor cell death is limited by a number of factors, including the adverse response of the tumor microenvironment to the treatment and either intrinsic or acquired mechanisms of evasive resistance, and the existence of cancer stem cells CSCs.
Because of the central role of transcription factor nuclear factor-κB NF-κB in pancreatic cancer, we investigated the roles of NF-κB in apigenin-induced growth inhibition in pancreatic cancer cells. It showed that apigenin reduced cell growth and induced apoptosis in the cells. Moreover, IKK blockage potentiated the anticancer efficacy of apigenin and IKK-β overexpression attenuated the apigenin-induced cell growth inhibition.
Introduction Hepatocelluar carcinoma HCC represents one of the most common cancer types in the world. The standard treatment options for Pancreatic cancer xenograft mouse model often involve radiation- and chemo-therapy.
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Despite advances in the detection and treatment of the disease, mortality rate remains high because current therapies are limited by the emergence of radiation- and chemo-therapy-resistant cancer cells. Existing radiation-therapies against HCC are usually developed against the bulk of the tumor mass, where although they are able to initially shrink the size of the tumor, they fail to eradicate the lesion in full, thus resulting in disease relapse.
Recently, HCC progression has been thought to be driven by cancer stem cells CSC through their capacity for self-renewal, production of heterogeneous progeny, and resistance to radiation-therapy and to limitlessly divide. Therefore, clarification of the radioresistance mechanism is essential for developing novel therapeutic modalities to sensitize hepatoma cells to radiation and improve patient survival. CSCs are a subpopulation of tumors that are responsible for tumor maintenance and spreading.
These cells are characterized to possess unlimited proliferation potential, self-renewal ability, and differentiation capability to generate progenies that constitute the major tumor population [ 2 ]. The existence of CSCs has been described in a variety of hematologic and solid tumors including those of the breast, brain, colon, pancreas, lung, liver, and esophagus. CSCs are resistant to many current cancer pancreatic cancer xenograft mouse model, including chemo- and hpv virus is therapy [ 3 ].
In addition to driving tumorigenesis, CSCs might contribute to distant pancreatic cancer xenograft mouse model and disease relapse [ 4 ].
This suggests that the standard interventions, while killing the bulk of tumor cells, may ultimately fail because they do not eliminate CSCs but represent a selection pressure for CSCs. Since CSCs share similarities with stem cells, stem cell-associated surface markers have been used to identify and isolate CSCs in vitro.
In addition, CSCs can form spherical colonies in suspension cultures characterized and termed tumorspheres. Importantly, isolated CSCs exhibit increased resistance to chemotherapeutic agent and ionizing radiation [ 2 ].
Therefore, CSCs have become an important target for drug development. Pterostilbene has attracted much attention because it has been demonstrated to have both chemopreventive activity and tumor-killing effects similar to those of resveratrol.
For instance, pterostilbene was indicated to induce cell cycle arrest and apoptosis in a variety of cancer cell lines including lung, liver, breast, and pancreas [ 7 ]. Pancreatic cancer xenograft mouse model, it has been reported that pterostilbene prevents azoxymethane- AOM- induced colon tumorigenesis in mice via suppressing cancer cell proliferation and the induction pancreatic cancer xenograft mouse model apoptotic pathways [ 8 ].
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In addition, several pharmacological properties of pterostilbene make it an ideal anticancer agent for development. Structurally, pterostilbene contains two methoxy groups and one hydroxyl group as compared to those of resveratrol which has three hydroxyl groups.
The two methoxy groups substantially increase the lipophilicity and oral absorption of pterostilbene leading to a higher potential for cellular uptake. Furthermore, pterostilbene's half-life is also seven pancreatic cancer xenograft mouse model longer than resveratrol, min versus 14 min [ 10 ]. Collectively, pterostilbene possesses many desired anticancer properties for the development as potential clinical agent.
Materials and Methods 2. Materials Pterostilbene 3,5-dimethoxyhydroxystilbene, Pterostilbene was dissolved in DMSO and further diluted in sterile culture medium immediately prior to use.
Cell culture and subsequent experiments were used and carried out according to the guidelines established by Environmental and Experimental Safety Committee, Taipei Medical University, Taiwan.
The cells were placed on a 1 cm bolus and treated with a posterior-anterior direction portal to allow a 1 cm radiation buildup. A radiation absorption doses from 1, 5, and 10 Gy per single fraction were delivered to Mahlavu cells. Surviving cells were subsequently cultured and subjected to flow cytometric analysis.
Cells were gated on low side scatter, low-to-moderate forward scatter, and low PI. For data acquisition, at least 10, events were analyzed. The cells were then seeded into the upper chambers of matrigel coated filter inserts.
After incubating for 24 h at 37°C, filter inserts were removed from the wells, the cells that invaded or migrated through the membrane were stained with propidium iodide and fluorescence images were taken. To measure the migratory ability, cells were seeded into a Boyden chamber with 8 mm pore polycarbonate filters, which were not coated with matrigel.
Different concentrations of pterostilbene were used for the evaluation. The migration assay was measured as described in the invasion assay. The membranes were sequentially detected with an pancreatic cancer xenograft mouse model peroxidase-conjugated secondary antibody. Student's t-test was used to determine the statistical significance of the differences between experimental groups; P values pancreatic cancer xenograft mouse model than 0.
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The level of statistical significance was set at 0. Results 3. Mahlavu cells were irradiated with increasing dose of γ-radiation from 1 to 10 Hpv causes of cancer and subjected to flow cytometric analysis for CD expression.