Dehydrocorydaline inhibits the tumorigenesis of breast cancer MDA‑MB‑231 cells

Huang,Ying; Huang,Hui; Wang,Shiying; Chen,Feixiang; Zheng,Gang

doi:10.3892/mmr.2020.11122

July-2020 Volume 22 Issue 1

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July-2020 Volume 22 Issue 1

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Article Open Access

Dehydrocorydaline inhibits the tumorigenesis of breast cancer MDA‑MB‑231 cells

Authors:
- Ying Huang
- Hui Huang
- Shiying Wang
- Feixiang Chen
- Gang Zheng
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Affiliations: Department of Oncology, The Fifth Hospital of Wuhan, Wuhan, Hubei 430050, P.R. China, Department of Anesthesiology, The Fifth Hospital of Wuhan, Wuhan, Hubei 430050, P.R. China, Department of General Surgery, The Fifth Hospital of Wuhan, Wuhan, Hubei 430050, P.R. China

Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 43-50
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Published online on: May 5, 2020

https://doi.org/10.3892/mmr.2020.11122
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Abstract

Dehydrocorydaline (DHC) is an alkaloid isolated from Corydali syanhusuo that exhibits antitumor properties. It has been reported that DHC can inhibit the proliferation of breast cancer cells, however the underlying molecular mechanism remains elusive. Therefore, the main objective of this study was to evaluate the antitumor activity of DHC, and gain further insights into its mechanism of action. The viability of MDA‑MB‑231 cells was determined through a Cell Counting Kit‑8 assay. The effect of DHC on the proliferation of MDA‑MB‑231 cells was detected by flow cytometry and 5‑ethynyl‑2'‑deoxyuridine staining. Apoptosis was evaluated by Annexin V‑FITC and PI staining through flow cytometry. The impact of DHC treatment on the colony‑forming ability of breast cancer cells was assessed. The expression levels of proliferation‑associated genes cyclin‑dependent kinases 1 (CDK1) and cyclin D1 (CCND1) and apoptosis‑related genes BCL2 and caspases 3/8/9 were quantified by real‑time PCR. Western blot analysis was performed to evaluate the production of cleaved caspase 3/9 and matrix metalloproteinase (MMP)2/9. DHC‑treated MDA‑MB‑231 cells were subcutaneously injected into mice. Subsequent immunohistochemical analyses were performed. DHC inhibited the viability, proliferation, colony‑forming ability and migration of MDA‑MB‑231 cells; in addition, DHC treatment promoted their apoptosis. DHC inhibited the production of proliferation‑ and anti‑apoptosis‑associated proteins CDK1, CCND1, BCL2 as well as that of the metastasis‑associated proteins MMP2 and MMP9. However, it promoted the expression of the pro‑apoptotic caspases 3/8/9. Moreover, DHC inhibited the growth of MDA‑MB‑231 tumor xenografts in SCID mice, and decreased cell proliferation in newly formed tumors in vivo. DHC exerted anticancer effects by downregulating cell proliferation, antiapoptosis, metastasis‑associated proteins CDK1, CCND1, BCL2 and metastasis‑associated proteins MMP2 and MMP9, and by upregulating the expression of proapoptotic proteins caspase 3/8/9.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Dehydrocorydaline inhibits the tumorigenesis of breast cancer MDA‑MB‑231 cells

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