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Orthotopic Injection of Breast Cancer Cells into the Mice Mammary Fat Pad
Published on: January 20, 2019
Compound Opening Arrow Mixture exerts anti-tumor effects in a mouse model of breast cancer
Zhen Zhou1, Yanfang Peng1, Wang Ai1
1Deparment of Traditional Chinese Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China.
Abstract:
Compound Opening Arrow Mixture (COAM) has demonstrated therapeutic effects in patients with breast cancer. We explored the underlying molecular mechanisms of COAM using a mouse model of breast cancer. Luciferase-labeled 4T1-Luc2 cells were inoculated into the breast pad of BALB/c-nu mice, which were divided into model group (saline), COAM (6 g/ml high-dose, 3 g/ml medium-dose, and 1.5 g/ml low-dose) groups, and low-molecular-weight heparin (LMWH, 1500 U/Kg) group. The number and distribution of 4T1-luc2 tumors were measured by an in vivo imaging system. Tumor cell apoptosis was measured through TUNEL and quantitating the expression of Caspase-3 mRNA and protein. Compared with the model group, in vivo tumor growth was lower in the LMWH- and COAM-treated groups. Tumor apoptosis was time-dependent and dose-dependent, as shown by a higher TUNEL apoptotic index and higher Caspase-3 mRNA and Caspase-3/cleaved-Caspase-3 proteins levels on the 14th day than the 7th day. The COAM high-dose group had the highest apoptotic index and the most activation of Caspase-3. Collectively, COAM significantly inhibits the growth of 4T1-luc2 breast cancer in mice and induces tumor apoptosis by activating Caspase-3, which provides a preliminary explanation of therapeutic effects of COAM.
Insights
Compound Opening Arrow Mixture (COAM) effectively inhibits breast cancer growth in mice by inducing tumor cell apoptosis. This mechanism involves the activation of Caspase-3, offering insights into COAM's therapeutic potential.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Compound Opening Arrow Mixture (COAM) shows promise for breast cancer treatment.
- Understanding the molecular mechanisms of COAM is crucial for its therapeutic application.
Purpose of the Study:
- To investigate the molecular mechanisms behind the therapeutic effects of COAM in a mouse model of breast cancer.
- To evaluate the impact of COAM on tumor growth and apoptosis.
Main Methods:
- Utilized a mouse model with luciferase-labeled 4T1-Luc2 breast cancer cells.
- Administered varying doses of COAM and low-molecular-weight heparin (LMWH).
- Assessed tumor growth using in vivo imaging and measured apoptosis via TUNEL assay and Caspase-3 expression analysis.
Main Results:
- COAM treatment significantly reduced in vivo tumor growth compared to the control group.
- Tumor apoptosis was observed to be both time- and dose-dependent.
- The high-dose COAM group exhibited the highest apoptotic index and greatest Caspase-3 activation.
Conclusions:
- COAM demonstrates significant inhibition of 4T1-luc2 breast cancer growth in mice.
- COAM induces tumor apoptosis through the activation of Caspase-3.
- These findings provide a preliminary molecular explanation for COAM's therapeutic efficacy in breast cancer.
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