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Int. J. Mol. Sci. 2017, 18(1), 132; doi:10.3390/ijms18010132

Icaritin Reduces Oral Squamous Cell Carcinoma Progression via the Inhibition of STAT3 Signaling

1
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China
2
Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China
*
Author to whom correspondence should be addressed.
Academic Editor: Terrence Piva
Received: 21 November 2016 / Revised: 20 December 2016 / Accepted: 6 January 2017 / Published: 12 January 2017
(This article belongs to the Section Bioactives and Nutraceuticals)
View Full-Text   |   Download PDF [14401 KB, uploaded 13 January 2017]   |  

Abstract

Icaritin, a traditional Chinese medicine, possesses antitumor activity. The current study aimed to investigate icaritin effect and potential mechanism on oral squamous cell carcinoma (OSCC) development. OSCC cells proliferation, apoptosis, and autophagy were analyzed after incubation with icaritin at different concentrations and incubation times. The expressions of proteins related to proliferation, apoptosis, and autophagy, as well as signal transducer and activator of transcription 3 (STAT3) signal network, were also evaluated by western blot. Furthermore, STAT3 was knocked down by siRNA transfection to determine STAT3 role in OSCC cell proliferation and apoptosis. An oral specific carcinogenesis mouse model was used to explore icaritin effect on OSCC in vivo. Icaritin significantly inhibited OSCC proliferation in vitro and reduced the expression of both the cell-cycle progression proteins cyclin A2 and cyclin D1. Besides, icaritin increased cleaved caspase 3 and cleaved poly-(ADP-ribose) polymerase expression leading to apoptosis, and it activated autophagy. Icaritin significantly inhibited the expression of phospho-STAT3 (p-STAT3) in a dose- and time-dependent manner. In the in vivo experiment, the number of malignant tumors in the icaritin-treated group was significantly lower than the control. Overall, icaritin suppressed proliferation, promoted apoptosis and autophagy, and inhibited STAT3 signaling in OSCC in vitro and in vivo. In conclusion, icaritin might be a potential therapeutic agent against OSCC development. View Full-Text
Keywords: icaritin; oral squamous cell carcinoma; signal transducer and activator of transcription 3; premalignant lesion icaritin; oral squamous cell carcinoma; signal transducer and activator of transcription 3; premalignant lesion
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Yang, J.-G.; Lu, R.; Ye, X.-J.; Zhang, J.; Tan, Y.-Q.; Zhou, G. Icaritin Reduces Oral Squamous Cell Carcinoma Progression via the Inhibition of STAT3 Signaling. Int. J. Mol. Sci. 2017, 18, 132.

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