Document Type : Original Research Article
Authors
1
Master of midwifery Researcher and Lecturer Universidade Nacional Timor Lorosae, Dili, Timor Lorosae
2
Department of pathological analysis, collage of applied sciences, University of Fallujah Al-Anbar, Iraq
3
Department of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India
4
Department of Sciences, Vivekananda Global University, Jaipur, Rajasthan-303012, India
5
Department of Basic Science & Humanities, Raghu Engineering College, Visakhapatnam, India
6
Department of Pharmacy, Kut University College, Kut 52001, Wasit, Iraq
7
Advanced Research Center, Kut University College, Kut 52001, Wasit, Iraq
8
Pharmacy Department, Tishk International University, Erbil, Kurdistan Region, Iraq
9
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Sakaka-72388, Aljouf, Saudi Arabia
10
Department of Pharmaceutics, Al-Nisour University College, Baghdad/Iraq
11
Department of Pharmaceutical Chemistry, College of Pharmacy, University of Mosul, Mosul-41001, Iraq
Abstract
Objective: Triple-negative breast cancer (TNBC) is the most metastatic type of breast cancer. Cynaropicrin, a sesquiterpene lactone, shows potential anticancer effects. This study evaluated cynaropicrin's impact on metastasis and angiogenesis in TNBC cells.
Materials and Methods: MDA-MB-231 and MDA-MB-468 cell lines were exposed to incrementing concentrations of cynaropicrin. The proliferation of the cell lines was assayed using the MTT method. A wound scratch technique was chosen to appraise the migratory properties of cells following cynaropicrin treatment. The transcript levels of epithelial-mesenchymal transition (EMT) and pro-angiogenic factors were quantified via quantitative polymerase chain reaction. The western blotting technique estimated the amount of E-cadherin, N-cadherin, Fibronectin, Vimentin, and VEGFA.
Results: The proliferation of MDA-MB-231 and MDA-MB-468 cells was significantly lowered due to cynaropicrin in a concentration-associated way. Results of the wound healing method uncovered that cynaropicrin could mitigate the migration of breast-derived MDA-MB-231 and MDA-MB-468 cells. Cynaropicrin also upregulated E-cadherin and hindered the protein expression of N-cadherin, Vimentin, Fibronectin 1, and VEGFA in breast-derived MDA-MB-468 and MDA-MB-231 cells.
Conclusion: The present findings indicated the anti-metastatic capacity of cynaropicrin against TNBC by a mechanism that implicated the inhibition of the EMT and pro-angiogenic factor VEGFA. These outcomes suggest cynaropicrin as an anti-metastatic and anti-angiogenic sesquiterpene lactone against TNBC.
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