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28 October 2017 : Animal Research  

Scutellarin Inhibits Proliferation, Invasion, and Tumorigenicity in Human Breast Cancer Cells by Regulating HIPPO-YAP Signaling Pathway

Lengchen Hou1ABCD, Lei Chen1AF, Lin Fang1AEFG*

DOI: 10.12659/MSM.904492

Med Sci Monit 2017; 23:5130-5138

Abstract

BACKGROUND: The present study aimed to investigate the effects of Scutellarin on proliferation, invasion and tumorigenicity in human breast carcinoma MCF-7 cells and its associated molecular mechanisms.

MATERIAL AND METHODS: The MCF-7 cells were cultured with varies of concentrations of Scutellarin in vitro. The proliferation, invasion, and apoptosis of MCF-7 cells were studied via CCK-8 assay, transwell assay, and flow cytometry. In vivo expression of the HIPPO pathway key proteins YAP and p-YAP of MCF-7 cells were analyzed by immunohistochemistry.

RESULTS: The inhibition rates of Scutellarin-treated MCF-7 cells were 40.1%, 58.7%, and 70.6% for 24, 48, and 72 h, respectively. The MCF-7 cell proliferation was significantly inhibited by Scutellarin. Treating MCF-7 cells with Scutellarin led to invasion inhibition. The rates apoptotic cells were between 12.4±1.9% and 23.9±2.1% in 40–120 µM Scutellarin-administrated groups, which had a significant rise compared with the control group (7.8±1.9%, P<0.05). Scutellarin significantly inhibited MCF-7 xenograft tumor growth. Immunohistochemical analysis showed that the inhibition of tumor growth in Scutellarin-treated mice was associated with increased p-YAP and decreased YAP expression in vivo.

CONCLUSIONS: Scutellarin-treated breast carcinoma MCF-7 cells had significantly inhibited growth and induced apoptosis, which is associated with induction of autophagy through regulation of the HIPPO-YAP signaling pathway, providing support to the clinical use of Scutellarin-based medication to achieve optimized outcome in patients with breast carcinoma.

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Dinah V. Parums ORCID logo

DOI: 10.12659/MSM.952454

Med Sci Monit 2026; 32:e952454

0:00

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750