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.
Highlights
Oral squamous cell carcinoma (OSCC), as one of the most common cancers in the world, is a major public health problem [1]
Recent studies revealed that signal transducer and activator of transcription 3 (STAT3) is constitutively activated and involved in the process of apoptosis resistance in many malignant tumors and
Recent studies revealed that signal transducer and activator of transcription 3 (STAT3) is constitutively activated and involved the process of apoptosis resistance in many malignant
Summary
Oral squamous cell carcinoma (OSCC), as one of the most common cancers in the world, is a major public health problem [1]. Despite recent therapeutic advances in oral cancer, the mortality and over five-year survival rates remain unchanged, which can be largely attributed to the local recurrences and distant metastasis [3,4]. The premalignant lesions are believed to have high risk associated with the progression to cancer [6]. Targeting these lesions may represent a good option to prevent tumor progression and reduce the incidence of OSCC. New and effective therapeutic agents guaranteeing safety and minimal toxicity are urgently required for OSCC prevention and treatment
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