Development and characterization of MCF7 mammary carcinoma xenografts in a non-immunocompromised rat model

Dunpall, Rekha; Opoku, Andy R.; Revaprasadu, Neerish

doi:10.4314/tjpr.v15i10.5

Cited by 5 publications

(4 citation statements)

References 18 publications

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“…Then the trypsinized cells were washed with serum-free medium twice before its resuspension into the matrigel-added serum-free medium (1:1). Each immunosuppressed mouse was injected with (2 × 10 6 tumor cells/0.2 mL) orthotopic intradermally [14,84] into the 4th mammary fat pad. When the tumor size grew up to approx.~150-250 mm 3 , the mice were randomly divided into different groups (according to experimental design).…”

Section: In Vivo Cytotoxic Activity In Xenografting Mice Model Inducementioning

confidence: 99%

Tioconazole and Chloroquine Act Synergistically to Combat Doxorubicin-Induced Toxicity via Inactivation of PI3K/AKT/mTOR Signaling Mediated ROS-Dependent Apoptosis and Autophagic Flux Inhibition in MCF-7 Breast Cancer Cells

et al. 2021

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Cancer is a complex devastating disease with enormous treatment challenges, including chemo- and radiotherapeutic resistance. Combination therapy demonstrated a promising strategy to target hard-to-treat cancers and sensitize cancer cells to conventional anti-cancer drugs such as doxorubicin. This study aimed to establish molecular profiling and therapeutic efficacy assessment of chloroquine and/or tioconazole (TIC) combination with doxorubicin (DOX) as anew combination model in MCF-7 breast cancer. The drugs are tested against apoptotic/autophagic pathways and related redox status. Molecular docking revealed that chloroquine (CQ) and TIC could be potential PI3K and ATG4B pathway inhibitors. Combination therapy significantly inhibited cancer cell viability, PI3K/AkT/mTOR pathway, and tumor-supporting autophagic flux, however, induced apoptotic pathways and altered nuclear genotoxic feature. Our data revealed that the combination cocktail therapy markedly inhibited tumor proliferation marker (KI-67) and cell growth, along with the accumulation of autophagosomes and elevation of LC3-II and p62 levels indicated autophagic flux blockage and increased apoptosis. Additionally, CQ and/or TIC combination therapy with DOX exerts its activity on the redox balance of cancer cells mediated ROS-dependent apoptosis induction achieved by GPX3 suppression. Besides, Autophagy inhibition causes moderately upregulation in ATGs 5,7 redundant proteins strengthened combinations induced apoptosis, whereas inhibition of PI3K/AKT/mTOR pathway with Beclin-1 upregulation leading to cytodestructive autophagy with overcome drug resistance effectively in curing cancer. Notably, the tumor growth inhibition and various antioxidant effects were observed in vivo. These results suggest CQ and/or TIC combination with DOX could act as effective cocktail therapy targeting autophagy and PI3K/AKT/mTOR pathways in MCF-7 breast cancer cells and hence, sensitizes cancer cells to doxorubicin treatment and combat its toxicity.

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Section: In Vivo Cytotoxic Activity In Xenografting Mice Model Inducementioning

confidence: 99%

Tioconazole and Chloroquine Act Synergistically to Combat Doxorubicin-Induced Toxicity via Inactivation of PI3K/AKT/mTOR Signaling Mediated ROS-Dependent Apoptosis and Autophagic Flux Inhibition in MCF-7 Breast Cancer Cells

et al. 2021

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“…Later, after counting, a volume of 1 ml containing 1 × 10 7 MCF-7 cells was injected around the teat of the mammary gland intradermally. To initiate tumor formation, rats were given intramuscular estrogen injections (0.01 ml/kg body weight, Folon 5 mg/ml) twice a day before receiving the MCF-7 injection, which typically took about four weeks 16 , 26 .…”

Section: Methodsmentioning

confidence: 99%

“…It is an affordable byproduct that contains essential bioflavonoids found in citrus fruits like lemon and orange 15 . Hes has a variety of health benefits, including anti-allergic, anti-oxidant, and anti-inflammatory properties 16 . Also, it has anticarcinogenic effects in the tongue, esophagus, colon, and urinary bladder in rat carcinogenesis models 17 .…”

Section: Introductionmentioning

confidence: 99%

Synergistic effects of bee venom, hesperidin, and piperine with tamoxifen on apoptotic and angiogenesis biomarker molecules against xerographic MCF-7 injected rats

Khamis,

Ali,

Salim

et al. 2024

Sci Rep

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Breast cancer ranks as the second leading most significant of mortality for women. Studies have demonstrated the potential benefits of natural compounds in cancer treatment and prevention, either in isolation or in conjunction with chemotherapy. In order to improve Tamoxifen's therapeutic efficacy in in-vivo studies, our research sought to determine the effects of hesperidin, piperine, and bee venom as natural compounds, as well as their combination effect with or without Tamoxifen. First, 132 female albino rats were equally divided into six groups and five subgroups, and breast cancer was induced in the selected groups by xenografting of MCF7 cells. Second, the effect of single and best ratio combinations treatment from previous in vitro studies were selected. Next, tumorous mammary glands were collected for apoptotic and antiapoptotic biomarkers and cell cycle analysis. Single or combined natural products with or without Tamoxifen revealed a significant up-regulation in apoptotic genes Bax and Casp3 and a downregulation of antiapoptotic and angiogenesis genes Bcl-2 and VEGF genes. We found that cell cycle arrest in the G0/G1 phase was exclusively caused by Tamoxifen and/ or hesperidin. However, the cell cycle arrest in the G2/M phase is a result of the combination of piperine and bee venom, with or without Tamoxifen by using the flow cytometric technique. Our research concludes that bee venom, hesperidin, and piperine can synergistically enhance to increase Tamoxifen's efficiency in the management of breast cancer.

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“…To enhance tumorigenesis, rats were intramuscularly injected with estrogen (Folon 5mg / ml, 0.01 ml / kg body weight) 1 day before MCF7 transplant and proceeded daily for ~ 3 weeks till tumor formation [22] . The tumor first appeared in the 4 th week of the experiment.…”

Section: Induction Of Breast Cancer Model By Xenografting Of Mcf7 Cellsmentioning

confidence: 99%

Differential expression profile for some genes and microRNAs associated with pathogenesis and progression of breast cancer

2020

jcbsc

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Breast cancer (BC) is the second cause of death after lung cancer in women all over the world. The main reasons for a lack of complete treatment for BC are the presence of many mysterious gaps in molecular signals regulating BC pathogenesis and progression. Herein, we studied the differential expression profile for some genes and microRNAs associated with the pathogenesis and progression of BC induced by xenografting of MCF7 cells in rats. Female albino rats (n = 7/group) were randomly divided into two groups: group 1 served as a normal control group and group 2 (tumor group) injected with MCF7 cells (2x10 7 cells in the 200 µL PBS) twice intradermally around the right thoracic teat of the mammary gland at the 5 th and the 12 th day of the experiment. Tumorous mammary glands samples were collected for molecular analysis by real time PCR. The obtained data revealed a significant decrease in the expression of breast cancer suppressor genes [Breast Cancer gene 1 (BRCA1), BRCA2, and p53] and a significant increase in their suppressor microRNAs (miRNAs) [miRNA-146a and miRNA-182 (targeting BRCA1), miRNA19a (targeting BRCA2), and miRNA-125b and miR-504 (targeting p53)] in tumorous tissues. Moreover, the expression of genes related to inhibition of epithelial mesenchymal Differential expression……. Marwa E. Yousef et al.

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Development and characterization of MCF7 mammary carcinoma xenografts in a non-immunocompromised rat model

Abstract: Purpose: To investigate the development of mammary tumours in female Sprague-dawley rats through a simple subcutaneous injection of human adenocarcinoma breast cells (MCF7) in combination with basement membrane matrix (BME

Cited by 5 publications

References 18 publications

Tioconazole and Chloroquine Act Synergistically to Combat Doxorubicin-Induced Toxicity via Inactivation of PI3K/AKT/mTOR Signaling Mediated ROS-Dependent Apoptosis and Autophagic Flux Inhibition in MCF-7 Breast Cancer Cells

Tioconazole and Chloroquine Act Synergistically to Combat Doxorubicin-Induced Toxicity via Inactivation of PI3K/AKT/mTOR Signaling Mediated ROS-Dependent Apoptosis and Autophagic Flux Inhibition in MCF-7 Breast Cancer Cells

Synergistic effects of bee venom, hesperidin, and piperine with tamoxifen on apoptotic and angiogenesis biomarker molecules against xerographic MCF-7 injected rats

Differential expression profile for some genes and microRNAs associated with pathogenesis and progression of breast cancer

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