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Biomed Pharmacother. 2018 Jul;103:473-481. doi: 10.1016/j.biopha.2018.03.121. Epub 2018 Apr 24.

Sulforaphane promotes apoptosis, and inhibits proliferation and self-renewal of nasopharyngeal cancer cells by targeting STAT signal through miRNA-124-3p.

Author information

1
Henan Provincial People's Hospital, 7 Weiwu Road, Zhengzhou, Henan, 450003 China; University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0021 United States.
2
University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0021 United States.
3
Harvard Medical School, 55 Fruit Street Boston, MA, 02114 United States.
4
Henan Provincial People's Hospital, 7 Weiwu Road, Zhengzhou, Henan, 450003 China.
5
University of Illinois at Chicago College of Medicine, 1835 W Polk St, Chicago, IL, 60612 United States.
6
Henan Provincial People's Hospital, 7 Weiwu Road, Zhengzhou, Henan, 450003 China. Electronic address: GUANGZHI72@126.com.

Abstract

Sulforaphane (SF) exhibits an anti-tumor effect in a variety of cancers, but little is known about its function in nasopharyngeal carcinoma. SF could decrease the expression of stem cell markers, β-catenin, Nanog, c-Myc, Oct3/4 and Sox2 in nasopharyngeal cancer cells (HONE1 and SUN1), and inhibit the formation of tumor spheres. Moreover, SF inhibits proliferation and induces apoptosis decreasing the stemness of nasopharyngeal cancer cells through a mechanism related to STAT3 signaling in vitro. We found that SF inhibits total STAT3 expression level and STAT3 phosphorylation (troy 704 and troy 705) by upregulation of miRNA-124-3p. Our results provide the evidence for discovering the novel drugs against nasopharyngeal carcinoma, and potential drugs targeting STAT3 signaling pathway.

KEYWORDS:

Nasopharyngeal Cancer; STAT signal; Self-renewal; Sulforaphane; miRNA-124-3p

PMID:
29677532
DOI:
10.1016/j.biopha.2018.03.121
[Indexed for MEDLINE]

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