scholarly journals Influence of a B16/F10 melanoma variant on the Вcl-2 levels in mitochondria in various organs of female mice

2021 ◽  
Vol 20 (3) ◽  
pp. 46-53
Author(s):  
O. I. Kit ◽  
E. M. Frantsiyants ◽  
I. V. Neskubina ◽  
N. D. Cheryarina ◽  
A. I. Shikhlyarova ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Development ◽  
Growth Period ◽  
Pathological Process ◽  
Intact Group ◽  
Kidney Mitochondria ◽  
Female Mice ◽  
Thermo Fisher Scientific ◽  
Liver And Kidney ◽  
Melanoma Growth

Aim. To study the Bcl-2 level in mitochondria of various organs in female mice with standard and stimulated growth of an experimental B16/F10 melanoma.Materials and methods. The study included С57ВL/6 female mice (n = 168). The experimental animals were divided into the following groups: an intact group (n = 21), a group with modelled chronic neuropathic pain (CNP) (n = 21), an M group with B16/F10 melanoma (n = 63), and a CNP + M group (n = 63). The Bcl-2 concentration (ng / mg protein) in mitochondrial samples was determined by ELISA (Thermo Fisher Scientific, Austria). Statistical analysis of the results was carried out using Statistica 10.0.Results. Compared to the Bcl-2 levels in the intact animals, CNP decreased this parameter in the cardiac mitochondria by 1.3 times, while increasing it by 5.9 times in the skin mitochondria. In the dynamics of standard melanoma growth, the Bcl-2 content changed compared with the corresponding intact values in the mitochondria of the brain, heart, and skin, but did not change in the liver and kidneys. In the mitochondria in melanoma, the Bcl-2 levels were high throughout the entire period of standard tumor growth in comparison with the intact skin. The stimulated melanoma growth in CNP was involving more organs into the pathological process as the tumor was growing. Thus, in comparison with the values in the CNP group, the mitochondrial Bcl-2 levels changed in the heart at week 1; in the heart and skin – at week 2; in the heart, skin, and brain – at week 3. The Bcl-2 levels did not change in the liver and kidney mitochondria. In the mitochondria in the CNP-stimulated melanoma, the Bcl-2 levels were lower than in the skin mitochondria in CNP throughout the entire tumor growth period.Conclusion. The liver and kidney mitochondria are somewhat Bcl-2 stable in both standard and stimulated tumor growth. It is assumed that different Bcl-2 dynamics in the mitochondria in melanoma depending on the variant of tumor development reflects the modulating effect of CNP and the ability to change the Bcl-2 levels according to the growth phase.

scholarly journals Influence of B16/F10 melanoma growth variant on calcium levels in mitochondria in various organs of female mice

2021 ◽  
Vol 8 (1) ◽  
pp. 20-29
Author(s):  
O. I. Kit ◽  
E. M. Frantsiyants ◽  
I. V. Neskubina ◽  
E. I. Surikova ◽  
I. V. Kaplieva ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Cells ◽  
Pain Syndrome ◽  
Neurogenic Pain ◽  
Intact Group ◽  
Female Mice ◽  
Terminal Stage ◽  
Initial Stage ◽  
The Brain ◽  
Melanoma Growth

Purpose of the study. To analyze the calcium levels in mitochondria of cells in different organs in standard and stimulated growth of experimental В16/F10 melanoma. Materials and Methods. The study included female С57ВL/6 mice (n=168). Experimental groups: intact group (n=21), group with a model of chronic neurogenic pain (CNP) (n=21), group M – B16/F10 melanoma (n=63), group M+CNP – mice (n=63) with transplantation of B16/F10 melanoma 3 weeks after CNP model creation. The concentration of calcium in mitochondrial samples was determined by a biochemical method (Abris+, Russia). Results were statistically analyzed using the Statistica 10.0 program. Results. CNP decreased calcium levels in mitochondria of cells in the brain by 1.4 (р=0.00153) times, liver by 2.6 times and heart by 3.2 times and increased the levels in the skin by 97.1 times. In standard growth of experimental melanoma, levels of calcium in cell mitochondria in most of the studied organs increased at the initial stage of the melanoma growth, and decreased to intact values and lower by the terminal stage. In the mitochondria of tumor cells, calcium levels were stably high at all stages of standard tumor growth. At the initial stage of CNP‑stimulated tumor growth, a decrease in calcium in the mitochondria of the skin by 5.7 times and its accumulation in the mitochondria of the brain by 6.6 times, heart, and kidneys were recorded by 1.5 times. At the terminal stage of stimulated melanoma growth, extremely low calcium values were recorded in the mitochondria of all organs. A stably low level of calcium was registered in the mitochondria of tumor cells at all stages of stimulated melanoma growth. Conclusions. The growth of experimental B16/F10 melanoma in female mice is accompanied by mitochondrial dysfunction affecting most organs. Stimulation of the growth of experimental melanoma with chronic neurogenic pain, unlike the standard growth variant, changes accumulation of calcium in the mitochondria of cells both in organs and in the tumor itself. The chronic pain syndrome accompanying a malignant process can influence its course with the involvement of mitochondria and the modification of their functions.

Comorbidity affects Вcl-2 levels in mitochondria in C57BL/6 mice with transplantable B16/F10 melanoma.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21581-e21581
Author(s):  
Irina V. Neskubina ◽  
Elena M. Frantsiyants ◽  
Valeria A. Bandovkina ◽  
Natalia D. Cheryarina ◽  
Alla I. Shikhlyarova ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Development ◽  
Brain Mitochondria ◽  
The Body ◽  
Heart Mitochondria ◽  
Control Group ◽  
Neurogenic Pain ◽  
Intact Group ◽  
Vital Functions ◽  
Thermo Fisher Scientific

e21581 Background: Overexpression of the Bcl-2 protein inhibits apoptosis and promotes carcinogenesis. Stress causes signaling leading to cell buffering with Bcl-2 protein above acceptable levels. The purpose of the study was to analyze the influence of comorbidity – chronic neurogenic pain (CNP) – on the Bcl-2 levels in mitochondria of cells of melanoma, the heart, skin and brain in female mice with growing tumors. Methods: Female С57ВL/6 mice were divided into groups: intact group (n = 21); control group with a CNP model – bilateral sciatic nerve ligation (n = 21); group M – B16/F10 melanoma (n = 63); CNP+M group – B16/F10 melanoma was transplanted 3 weeks after the CNP model creation (n = 63). The concentration of Bcl-2 (ng/mg of protein) was determined in mitochondrial samples by ELISA (Thermo Fisher Scientific, Austria). Statictical analysis of results: Statistica 10.0. Results: CNP decreased the Bcl-2 level in heart mitochondria by 1.3 times (p < 0.05), but increased it in skin and brain mitochondria by 5.8 and 1.3 times, respectively. Similar changes were observed in melanoma growth 1 week after its transplantation: Bcl-2 levels decreased in heart mitochondria by 1.3 times, and increased in the skin and brain by 8.9 and 1.3 times, respectively. After 2 weeks of the tumor growth, Bcl-2 in brain mitochondria decreased by 1.7 times, and it started declining in the skin by the 3rd week – by 4 times, compared to intact females. Bcl-2 in tumor mitochondria exceeded the values in the skin by more than 4 times throughout the experiment. Tumor growth in presence of CNP caused a decrease in Bcl-2 in brain mitochondria by 2.4 times after 3 weeks, and in the heart and skin – by 2 and 1.7 times, respectively, after 2 weeks. Bcl-2 in tumor mitochondria in presence of CNP was lower than in the intact skin on average by 1.8 times throughout the experiment. Conclusions: CNP as a comorbidity caused a modulating effect on the mechanisms of survival and apoptosis of cells both in the tumor and in the main organs providing the vital functions of the body - the brain and heart, and also affects the target organ of melanoma - the skin. The results demonstrated the ability of comorbidity to change levels of Bcl-2 in mitochondria depending on the stage of tumor development.

scholarly journals Increased Tumor Growth in Mice with Diet-Induced Obesity: Impact of Ovarian Hormones

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5826-5834 ◽  
Author(s):  
Shoshana Yakar ◽  
Nomeli P. Nunez ◽  
Patricia Pennisi ◽  
Pnina Brodt ◽  
Hui Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Tumor Growth ◽  
Glucose Intolerance ◽  
Tumor Development ◽  
Tumor Growth Rate ◽  
Obese Mice ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Body Adiposity ◽  
Obese Female

Obesity increases the risk of many cancers in both males and females. This study describes a link between obesity, obesity-associated metabolic alterations, and the risk of developing cancer in male and female mice. The goal of this study was to evaluate the relationship between gender and obesity and to determine the role of estrogen status in obese females and its effect on tumor growth. We examined the susceptibility of C57BL/6 mice to diet-induced obesity, insulin resistance/glucose intolerance, and tumors. Mice were injected sc with one of two tumorigenic cell lines, Lewis lung carcinoma, or mouse colon 38-adenocarcinoma. Results show that tumor growth rate was increased in obese mice vs. control mice irrespective of the tumor cell type. To investigate the effect of estrogen status on tumor development in obese females, we compared metabolic parameters and tumor growth in ovariectomized (ovx) and intact obese female mice. Obese ovx female mice developed insulin resistance and glucose intolerance similar to that observed in obese males. Our results demonstrate that body adiposity increased in ovx females irrespective of the diet administered and that tumor growth correlated positively with body adiposity. Overall, these data point to more rapid tumor growth in obese mice and suggest that endogenous sex steroids, together with diet, affect adiposity, insulin sensitivity, and tumor growth in female mice.

Apoptosis indices in liver cell mitochondria in B16/F10 melanoma growing in presence of chronic neurogenic pain

2021 ◽  
pp. 71-79
Author(s):  
Е.М. Франциянц ◽  
И.В. Нескубина ◽  
Е.И. Сурикова ◽  
А.И. Шихлярова ◽  
В.А. Бандовкина ◽  
...  
Keyword(s):  
Cytochrome C ◽  
G Protein ◽  
Tumor Development ◽  
Mitochondrial Fraction ◽  
Liver Mitochondria ◽  
Caspase 9 ◽  
Neurogenic Pain ◽  
Intact Group ◽  
Subcutaneous Transplantation ◽  
Melanoma Growth

Введение. Печень по количеству, плотности митохондрий один из самых богатых органов, который также является критическим местом для множества метаболических путей. Цель исследования - изучение показателей апоптоза в митохондриях печени самок мышей линии С57ВL/6 при самостоятельном росте меланомы В16/F10 и на фоне коморбидной патологии - хронической нейрогенной боли. Методика. В эксперименте использовали мышей-самок (n=168) линии С57ВL/6. Группы: интактная (n=21); контрольная (n=21) - создание модели хронической нейрогенной боли (ХНБ), путем двусторонней перевязки седалищных нервов; группа сравнения (n=63) - подкожная трансплантация меланомы B16/F10; основная группа (ХНБ+B16/F10) (n=63) - подкожная трансплантация меланомы В16/F10 через 3 нед после моделировия ХНБ. В митохондриях печени методом ИФА определяли концентрацию: цитохрома С (нг/г белка), каспазы 9 (нг/г белка), Bcl-2 (нг/г белка), AIF (нг/г белка), кальция (Са 2+) (мМоль/г белка). Результаты. В митохондриях клеток печени через 1 нед роста меланомы относительно интактных значений фиксировали нарастание уровней AIF в 2,2 раза, цитохрома С в 1,7 раза (р<0,05) и снижение каспазы 9 в 2,0 раза; через 3 нед - падение кальция в 4,7 раза, AIF в 7,1 раза и цитохрома С в 1,7 раза (р<0,05) и накопление каспазы 9 - 1,6 раза (р<0,05). Развитие опухоли при ХНБ через 1 нед сопровождалось уменьшением концентрации AIF в 29,3 раза и цитохрома С в 2,0 раза по сравнению с контрольными значениями (ХНБ). Через 3 недели роста меланомы на фоне ХНБ фиксировали снижение уровней AIF в 6,6 раза, цитохрома С в 4,7 раза и кальция в 32,8 раза, уровень каспазы 9, напротив, повышался в 1,5 раза (р<0,05). Заключение. Наличие коморбидной патологии - ХНБ при опухолевом процессе способствует раннему возникновению нарушений в электронно-транспортной цепи митохондрий клеток печени. Background. The liver is one of the richest organs in terms of the number and density of mitochondria; it is also a critical site for many metabolic pathways. The aim of the study was to analyze indicators of apoptosis in liver mitochondria in female С57ВL/6 mice with B16/F10 melanoma growing alone and in presence of chronic neurogenic pain. Methods. Female С57ВL/6 mice (n=168) were studied. Animals were divided into groups: intact group (n=21); controls (n=21) with a model of chronic neurogenic pain (CNP) created by bilateral sciatic nerve ligation; comparison group (n=63) with subcutaneous transplantation of B16/F10 melanoma; main group (CNP+B16/F10) (n=63) with subcutaneous transplantation of B16/F10 melanoma 3 wks after modeling CNP. Cytochrome C (ng/g protein), caspase-9 (ng/g protein), Bcl-2 (ng/g protein), AIF (ng/g protein), and calcium (Ca2+) (mmol/g protein) were measured by ELISA in the liver mitochondrial fraction. Results. After 1 wk of melanoma growth, AIF increased by 2.2 times, cytochrome C increased by 1.7 times (p<0.05), and caspase-9 decreased by 2.0 times compared to the intact group values. After 3 wks, calcium decreased by 4.7 times, AIF by 7.1 times, cytochrome C by 1.7 times (p<0.05), and caspase-9 increased by 1.6 times (p<0.05). After 1 wk, tumor development in the presence of CNP was accompanied by decreases in AIF by 29.3 times and cytochrome C by 2.0 times, compared to control CNP values. After 3 wks of melanoma growth in presence of CNP, AIF decreased by 6.6 times, cytochrome C by 4.7 times, and calcium by 32.8 times. Caspase-9, on the contrary, increased by 1.5 times (p<0.05). Conclusions. The presence of CNP comorbidity during the tumor development facilitates earlier occurrence of disorders in the electron transport chain of hepatocyte mitochondria.

scholarly journals Interaction between CD44 and hyaluronate is directly implicated in the regulation of tumor development.

1994 ◽  
Vol 180 (1) ◽  
pp. 53-66 ◽  
Author(s):  
A Bartolazzi ◽  
R Peach ◽  
A Aruffo ◽  
I Stamenkovic
Keyword(s):  
Tumor Growth ◽  
Cell Attachment ◽  
Tumor Development ◽  
Tumor Formation ◽  
Wild Type ◽  
Cd44 Isoforms ◽  
Secondary Tumor ◽  
Mediate Cell ◽  
Melanoma Growth

CD44 is implicated in the regulation of tumor growth and metastasis but the mechanism by which expression of different CD44 isoforms determines the rate of primary and secondary tumor growth remains unclear. In the present study we use a human melanoma transfected with wild-type and mutant forms of CD44 to determine which functional property of the CD44 molecule is critical in influencing tumor behavior. We show that expression of a wild-type CD44 isoform that binds hyaluronic acid augments the rapidity of tumor formation by melanoma cells in vivo, whereas expression of a CD44 mutant, which does not mediate cell attachment to hyaluronate, fails to do so. The importance of CD44-hyaluronate interaction in tumor development is underscored by the differential inhibitory effect of soluble wild-type and mutant CD44-Ig fusion proteins on melanoma growth in vivo. Whereas local administration of a mutant, nonhyaluronate binding, CD44-Ig fusion protein has no effect on subcutaneous melanoma growth in mice, infusion of wild-type CD44-Ig is shown to block tumor development. Taken together, these observations suggest that the tumor growth promoting property of CD44 is largely dependent on its ability to mediate cell attachment to hyaluronate.

scholarly journals The state of apoptosis factor system in mitochondria of skin and tumor cells in standard and stimulated growth of B16/F10 melanoma in female C57BL/6 mice

2021 ◽  
Vol 8 (1) ◽  
pp. 8-19
Author(s):  
E. M. Frantsiyants ◽  
I. V. Neskubina ◽  
E. I. Surikova ◽  
A. I. Shikhlyarova ◽  
I. V. Kaplieva ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Caspase 9 ◽  
Neurogenic Pain ◽  
Skin Cells ◽  
Similar Tendency ◽  
Thermo Fisher Scientific ◽  
Fisher Scientific ◽  
Melanoma Growth

Purpose of the study. Studying the dynamics of factors of apoptosis in mitochondria of skin and tumors cells in female mice with melanoma growth stimulated by chronic neurogenic pain. Material and methods. The study included female С57ВL/6 mice (n=56) with a model of chronic neurogenic pain (CNP) produced by the bilateral sciatic nerve ligation and with transplanted B16/F10 melanoma. After 1–3 weeks of the tumor growth, levels of cytochrome C, caspase‑9 (Bioscience, Austria), Bcl‑2 (Thermo Fisher Scientific, Austria), and AIF (RayBiotech, USA) were determined by ELISA, and levels of calcium (Са2+) were determined by the Arsenazo III method (Abris+, Russia) in mitochondria of tumors cells and skin not affected by the tumor growth. Results. In the CNP state, mitochondria of the skin cells showed a significant increase in Са2+ by 96.7 times, AIF by 1.4 times and Bcl‑2 by 5.9 times, while caspase‑9 decreased by 2.6 times, compared to the levels in intact mice. In the CNP‑stimulated melanoma growth, mitochondria of cells of the skin not affected by the tumor growth demonstrated a decrease in all studied indices, except caspase‑9 – its levels increased by 4.6 times after 3 weeks of the tumor growth. In mitochondria of the tumor cells within 1–3 weeks, levels of Са2+ decreased over time by 37.2–96.1 times, respectively, AIF by 49.4–2.0 times, Bcl‑2 by 3.0–1.5 times, cytochrome C by 15.3–8.8 times, and caspase‑9 increased by 1.7–4.4 times compared with the level in animals with pain. Conclusions. In general, the growth of melanoma stimulated by chronic pain and the standard melanoma growth were characterized by the opposite dynamics of levels of apoptosis factor both in mitochondria of skin cells and in mitochondria of tumor cells, with the exception of cytochrome C. Mitochondria of melanoma cells and of the unchanged skin have a similar tendency to change the levels of apoptosis factors, which may indicate their functioning in the conditions of the mitochondrial network at the level of one organ. Mitochondria of tumor cells provide the anti‑apoptotic state of the tumor itself and of the skin not affected by the malignant process, probably due to the stress state of the skin.

scholarly journals Investigating New Therapeutic Strategies Targeting Hyperinsulinemia's Mitogenic Effects in a Female Mouse Breast Cancer Model

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1701-1710 ◽  
Author(s):  
Ran Rostoker ◽  
Keren Bitton-Worms ◽  
Avishay Caspi ◽  
Zila Shen-Orr ◽  
Derek LeRoith
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Experimental Studies ◽  
Tumor Development ◽  
Treated Group ◽  
Tumor Growth Rate ◽  
Breast Cancer Patients ◽  
Mitogenic Effect

Abstract Epidemiological and experimental studies have identified hyperinsulinemia as an important risk factor for breast cancer induction and for the poor prognosis in breast cancer patients with obesity and type 2 diabetes. Recently it was demonstrated that both the insulin receptor (IR) and the IGF-IR mediate hyperinsulinemia's mitogenic effect in several breast cancer models. Although IGF-IR has been intensively investigated, and anti-IGF-IR therapies are now in advanced clinical trials, the role of the IR in mediating hyperinsulinemia's mitogenic effect remains to be clarified. Here we aimed to explore the potential of IR inhibition compared to dual IR/IGF-IR blockade on breast tumor growth. To initiate breast tumors, we inoculated the mammary carcinoma Mvt-1 cell line into the inguinal mammary fat pad of the hyperinsulinemic MKR female mice, and to study the role of IR, we treated the mice bearing tumors with the recently reported high-affinity IR antagonist-S961, in addition to the well-documented IGF-IR inhibitor picropodophyllin (PPP). Although reducing IR activation, with resultant severe hyperglycemia and hyperinsulinemia, S961-treated mice had significantly larger tumors compared to the vehicle-treated group. This effect maybe secondary to the severe hyperinsulinemia mediated via the IGF-1 receptor. In contrast, PPP by partially inhibiting both IR and IGF-IR activity reduced tumor growth rate with only mild metabolic consequences. We conclude that targeting (even partially) both IR and IGF-IRs impairs hyperinsulinemia's effects in breast tumor development while simultaneously sparing the metabolic abnormalities observed when targeting IR alone with virtual complete inhibition.

Sunitinib-ibuprofen drug interaction affects the pharmacokinetics and tissue distribution of sunitinib to brain, liver, and kidney in male and female mice differently

2015 ◽  
Vol 29 (4) ◽  
pp. 404-416 ◽  
Author(s):  
Christine Li Ling Lau ◽  
Sook Tyng Chan ◽  
Manimegahlai Selvaratanam ◽  
Hui Wen Khoo ◽  
Adeline Yi Ling Lim ◽  
...  
Keyword(s):  
Drug Interaction ◽  
Tissue Distribution ◽  
Male And Female ◽  
Female Mice ◽  
Liver And Kidney

Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects

2011 ◽  
Vol 114 (3) ◽  
pp. 651-662 ◽  
Author(s):  
Hsin-I Ma ◽  
Shih-Hwa Chiou ◽  
Dueng-Yuan Hueng ◽  
Lung-Kuo Tai ◽  
Pin-I Huang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Critical Role ◽  
Tumor Development ◽  
Primary Brain Tumor ◽  
Scid Mice ◽  
Therapeutic Effects ◽  
Glioblastoma Cells ◽  
Source Case ◽  
Cox 2

Object Glioblastoma, the most common primary brain tumor, has a poor prognosis, even with aggressive resection and chemoradiotherapy. Recent studies indicate that CD133+ cells play a key role in radioresistance and recurrence of glioblastoma. Cyclooxygenase-2 (COX-2), which converts arachidonic acid to prostaglandins, is over-expressed in a variety of tumors, including CD133+ glioblastomas. The COX-2–derived prostaglandins promote neovascularization during tumor development, and conventional radiotherapy increases the proportion of CD133+ cells rather than eradicating them. The aim of the present study was to investigate the role of celecoxib, a selective COX-2 inhibitor, in enhancing the therapeutic effects of radiation on CD133+ glioblastomas. Methods Cells positive for CD133 were isolated from glioblastoma specimens and characterized by flow cytometry, then treated with celecoxib and/or ionizing radiation (IR). Clonogenic assay, cell irradiation, cell cycle analysis, Western blot, and xenotransplantation were used to assess the effects of celecoxib alone, IR alone, and IR with celecoxib on CD133+ and CD133− glioblastoma cells. Three separate xenotransplantation experiments were carried out using 310 severe combined immunodeficient (SCID) mice: 1) an initial tumorigenicity evaluation in which 3 different quantities of untreated CD133– cells or untreated or pretreated CD133+ cells (5 treatment conditions) from 7 different tumors were injected into the striatum of 2 mice (210 mice total); 2) a tumor growth study (50 mice); and 3) a survival study (50 mice). For these last 2 studies the same 5 categories of cells were used as in the tumorigenicity (untreated CD133– cells, untreated or pretreated CD133+ cells, with pretreatment consisting of celecoxib alone, IR alone, or IR and celecoxib), but only 1 cell source (Case 2) and quantity (5 × 104 cells) were used. Results High levels of COX-2 protein were detected in the CD133+ but not the CD133− glioblastoma cells. The authors further demonstrated that 30 μM celecoxib was able to effectively enhance the IR effect in inhibiting colony formation and increasing IR-mediated apoptosis in celecoxib-treated CD133+ glioblastoma cells. Furthermore, reduction in radioresistance was correlated with the induction of G2/M arrest, which was partially mediated through the increase in the level of phosphorylated-cdc2. In vivo xenotransplant analysis further confirmed that CD133+-associated tumorigenicity was significantly suppressed by celecoxib treatment. Importantly, pretreatment of CD133+ glioblastoma cells with a combination of celecoxib and IR before injection into the striatum of SCID mice resulted in a statistically significant reduction in tumor growth and a statistically significant increase in the mean survival rate of the mice. Conclusions Celecoxib combined with radiation plays a critical role in the suppression of growth of CD133+ glioblastoma stemlike cells. Celecoxib is therefore a radiosensitizing drug for clinical application in glioblastoma.

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