- 【Updated on May 12, 2025】 Integration of CiNii Dissertations and CiNii Books into CiNii Research
- Trial version of CiNii Research Automatic Translation feature is available on CiNii Labs
- Suspension and deletion of data provided by Nikkei BP
- Regarding the recording of “Research Data” and “Evidence Data”
FL118, a novel camptothecin analogue, suppressed migration and invasion of human breast cancer cells by inhibiting epithelial-mesenchymal transition <i>via</i> the Wnt/β-catenin signaling pathway
-
- Yang Zhihong
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Ji Lixia
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Jiang Guohui
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Liu Ranran
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Liu Zhantao
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Yang Yuecheng
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Ma Qingxia
- Department of Pharmacology, School of Pharmacy, Qingdao University
-
- Zhao Hongqin
- Department of Pharmacology, School of Pharmacy, Qingdao University
Search this article
Description
<p>The aim of the current study was to investigate the effects of FL118, a novel camptothecin analogue, on migration and invasion of human breast cancer cells and the underlying mechanisms of those effects. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and a plate clone formation assay were used to examine inhibition of the proliferation of MDA-MB-231 cells by FL118. Cell cycle distribution was detected using flow cytometry. A wound healing assay and a transwell assay were performed to detect the effects of FL118 on migration and invasion of MDA-MB-231 cells, respectively. qRT-PCR, Western blotting, and immunocytochemistry were used to study the effects of FL118 on expression of epithelial-mesenchymal transition (EMT)-related molecules and Wnt/ β-catenin signaling components in MDA-MB-231 cells. The current results indicated that FL118 inhibited the proliferation, migration and invasion of MDA-MB-231 cells in a dose- and time-dependent manner. FL118 caused MDA-MB-231 cells to accumulate in the S phase. FL118 significantly suppressed the expression of vimentin while enhancing the expression of E-cadherin. Moreover, decreased expression of β-catenin and its targets survivin and cyclin Dl was detected in the nucleus of MDA-MB-231 cells. Taken together, the current results suggest that FL118 inhibited Wnt/β-catenin signaling, leading to suppressed EMT and decreased migration and invasion of breast cancer cells.</p>
Journal
-
- BioScience Trends
-
BioScience Trends 12 (1), 40-46, 2018
International Research and Cooperation Association for Bio & Socio-Sciences Advancement
