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Citrus limonin lacks the antichemotherapeutic effect in human models of breast cancer
Siva Somasundaram1, Janet Price, Karen Pearce
1Department of Biology, University of Houston-Victoria, Sugar Land, TX 77479, USA. somasundarams@uhv.edu
Background/Aims:
Chemicals that interfere with reactive oxygen species metabolism can act as potential candidates for the treatment of cancer. Some of the glucosides of citrus limonin inhibit the endogenously generated reactive oxygen species. The aim is to study the interactions of limonin with chemotherapy.
Methods:
Breast cancer cell lines MCF-7 (p53 wild type) and MDA-MB-231 (p53 mutant) as well as the nontumorigenic epithelial cell line MCF-10 were used to screen the effect of limonin at 1-, 5- and 10-µM concentrations with camptothecin for apoptosis and NFĸB, p38 and ERK-MAPK signaling kinase assays. The effect of cyclophosphamide and limonin on MDA MB 231 xenografts was also studied.
Results:
Our results indicate that limonin did not inhibit camptothecin-induced apoptosis in human breast cancer cells in vitro through noninterference of camptothecin-induced phosphorylation of p38 MAPK and ERK-MAPK. Using an in vivo model of human breast cancer, limonin in combination with cyclophosphamide was not found to inhibit the cyclophosphamide-induced tumor regression through a reduced mitotic index of tumor xenograft cells when compared to treatment with cyclophosphamide alone.
Conclusion:
Both in vitro and in vivo results suggest that limonin could be beneficial for breast cancer patients undergoing chemotherapy.
Insights
Limonin, a citrus compound, shows potential in breast cancer treatment. It did not interfere with chemotherapy-induced apoptosis or tumor regression, suggesting it may complement existing cancer therapies.
Area of Science:
- Oncology
- Pharmacology
- Natural Products Chemistry
Background:
- Reactive oxygen species (ROS) metabolism is a target for cancer treatment.
- Citrus limonin glucosides can inhibit endogenous ROS.
- Limonin's interaction with chemotherapy warrants investigation.
Purpose of the Study:
- To investigate the effects of limonin on breast cancer cell lines.
- To determine limonin's impact on chemotherapy-induced apoptosis and signaling pathways.
- To evaluate limonin's efficacy in combination with cyclophosphamide in vivo.
Main Methods:
- Utilized breast cancer cell lines (MCF-7, MDA-MB-231) and a non-tumorigenic line (MCF-10).
- Assessed limonin's effects on apoptosis and signaling kinases (NFκB, p38, ERK-MAPK) with camptothecin.
- Studied the in vivo effect of limonin and cyclophosphamide on MDA-MB-231 xenografts.
Main Results:
- Limonin did not inhibit camptothecin-induced apoptosis in vitro.
- Limonin did not interfere with p38 MAPK and ERK-MAPK phosphorylation.
- In vivo, limonin combined with cyclophosphamide did not hinder tumor regression compared to cyclophosphamide alone.
Conclusions:
- Limonin does not antagonize standard chemotherapy agents.
- Limonin may offer complementary benefits for breast cancer patients undergoing chemotherapy.
- Further research into limonin as an adjunct cancer therapy is supported.
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