European Journal of Gynaecological Oncology (EJGO) is published by IMR Press from Volume 40 Issue 1 (2019). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.
Cite this article
Effects of cyclopamine on the biological characteristics of human breast cancer MCF-7 cell line and its mechanism
1 Department of Breast Surgery, the First Affiliated Hospital of Liaoning Medical University, Jinzhou (China)
Eur. J. Gynaecol. Oncol. 2015, 36(4), 469–472; https://doi.org/10.12892/ejgo2670.2015
Published: 10 August 2015
Purpose: To observe the effects of cyclopamine on the biological characteristics of human breast cancer MCF-7 cell line and explore its mechanism. Materials and Methods: After human breast cancer MCF-7 cells were treated with different-concentration cyclopamine for different periods, MTT assay was used to detect the inhibitory effect of cyclopamine on MCF-7 cell proliferation, flow cytometry was used to determine the distribution of MCF-7 cell cycle and the effect of cyclopamine on MCF-7 apoptosis, and Western blot was used to measure the protein levels of cyclins D1 and p21 in MCF-7 cells. Results: In certain range, MCF-7 cell proliferation was inhibited by cyclopamine in a dose- and time-dependent manner, and the optimal inhibiting concentration was ten μmol/L and the optimal action time at 48 hours. With the time prolongation of cyclopamine action, the cells in G0/G1 phase were significantly increased, but the cells in S phase were significantly decreased (compared with blank control group, all p < 0.05). With the time prolongation of cyclopamine action, apoptosis rate of MCF-7 cells was also significantly increased (compared with blank control group, all p < 0.05). The level of cyclin D1 of MCF-7 cells was decreased, but cyclin p21 was increased (compared with blank control group, all p < 0.05). Conclusion: Cyclopamine inhibits MCF-7 cell proliferation via arresting MCF-7 cell transformation from G1 phase to S phase. This may be associated with the expressions of Hedgehog (Hh) signaling pathway-related cyclins.