Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells

Abstract Psoralen could inhibit the proliferation of human breast cancer cells, however, the molecular mechanism was unclear. We evaluated the anti-proliferative effects of psoralen by MTT, plate colony formation assay and cell cycle analysis in MCF-7 and MDA-MB-231 cells. The effects of psoralen on...

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Autores principales: Xiaohong Wang, Chengfeng Xu, Yitong Hua, Kai Cheng, Yingzhe Zhang, Jian Liu, Yong Han, Song Liu, Guoqiang Zhang, Shujian Xu, Zhenlin Yang
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Publicado: Nature Portfolio 2018
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spelling oai:doaj.org-article:b8361f6867eb4f2986ea1f3a4c7582022021-12-02T15:09:12ZPsoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells10.1038/s41598-018-32438-72045-2322https://doaj.org/article/b8361f6867eb4f2986ea1f3a4c7582022018-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-32438-7https://doaj.org/toc/2045-2322Abstract Psoralen could inhibit the proliferation of human breast cancer cells, however, the molecular mechanism was unclear. We evaluated the anti-proliferative effects of psoralen by MTT, plate colony formation assay and cell cycle analysis in MCF-7 and MDA-MB-231 cells. The effects of psoralen on activation of Wnt/β-catenin and the related target genes were examined by quantitative real-time PCR, western blotting and cell immunofluorescence. The tumor growth was conducted in BALB/c nude mice and the pathological changes of heart, liver and kidney were also observed. Our results demonstrate that psoralen significantly inhibited cell proliferation by inducing G0/G1 phase arrest in MCF-7 cells and G2/M phase arrest in MDA-MB-231 cells. The expression of Fra-1 was reduced and Axin2 was promoted both in MCF-7 and MDA-MB-231 cells after psoralen treatment. The cytoplasmic accumulation and nuclear translocation of β-catenin were significantly reduced by psoralen. Psoralen increased the levels of phospho-(Y142) β-catenin, while decreased the expression of total β-catenin and its downstream target Fra-1 in vitro and vivo. Moreover, psoralen didn’t cause any significant toxicity at the effective concentration. Overall, our results might provide theoretical basis for clinical application of psoralen in breast cancer.Xiaohong WangChengfeng XuYitong HuaKai ChengYingzhe ZhangJian LiuYong HanSong LiuGuoqiang ZhangShujian XuZhenlin YangNature PortfolioarticleBreast CancerCell CyclePsoralen TreatmentPlate Colony Formation AssayRelative Target GeneMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-7 (2018)
institution DOAJ
collection DOAJ
language EN
topic Breast Cancer
Cell Cycle
Psoralen Treatment
Plate Colony Formation Assay
Relative Target Gene
Medicine
R
Science
Q
spellingShingle Breast Cancer
Cell Cycle
Psoralen Treatment
Plate Colony Formation Assay
Relative Target Gene
Medicine
R
Science
Q
Xiaohong Wang
Chengfeng Xu
Yitong Hua
Kai Cheng
Yingzhe Zhang
Jian Liu
Yong Han
Song Liu
Guoqiang Zhang
Shujian Xu
Zhenlin Yang
Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
description Abstract Psoralen could inhibit the proliferation of human breast cancer cells, however, the molecular mechanism was unclear. We evaluated the anti-proliferative effects of psoralen by MTT, plate colony formation assay and cell cycle analysis in MCF-7 and MDA-MB-231 cells. The effects of psoralen on activation of Wnt/β-catenin and the related target genes were examined by quantitative real-time PCR, western blotting and cell immunofluorescence. The tumor growth was conducted in BALB/c nude mice and the pathological changes of heart, liver and kidney were also observed. Our results demonstrate that psoralen significantly inhibited cell proliferation by inducing G0/G1 phase arrest in MCF-7 cells and G2/M phase arrest in MDA-MB-231 cells. The expression of Fra-1 was reduced and Axin2 was promoted both in MCF-7 and MDA-MB-231 cells after psoralen treatment. The cytoplasmic accumulation and nuclear translocation of β-catenin were significantly reduced by psoralen. Psoralen increased the levels of phospho-(Y142) β-catenin, while decreased the expression of total β-catenin and its downstream target Fra-1 in vitro and vivo. Moreover, psoralen didn’t cause any significant toxicity at the effective concentration. Overall, our results might provide theoretical basis for clinical application of psoralen in breast cancer.
format article
author Xiaohong Wang
Chengfeng Xu
Yitong Hua
Kai Cheng
Yingzhe Zhang
Jian Liu
Yong Han
Song Liu
Guoqiang Zhang
Shujian Xu
Zhenlin Yang
author_facet Xiaohong Wang
Chengfeng Xu
Yitong Hua
Kai Cheng
Yingzhe Zhang
Jian Liu
Yong Han
Song Liu
Guoqiang Zhang
Shujian Xu
Zhenlin Yang
author_sort Xiaohong Wang
title Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
title_short Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
title_full Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
title_fullStr Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
title_full_unstemmed Psoralen induced cell cycle arrest by modulating Wnt/β-catenin pathway in breast cancer cells
title_sort psoralen induced cell cycle arrest by modulating wnt/β-catenin pathway in breast cancer cells
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/b8361f6867eb4f2986ea1f3a4c758202
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