1. Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling
- Author
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Hu Shanshan, Xiao Lan, Li Xia, Wang Huang, Yin Ling, and Zuo Meifang
- Subjects
0301 basic medicine ,STAT3 Transcription Factor ,Medicine (General) ,proliferation ,Mice, Nude ,Uterine Cervical Neoplasms ,Biochemistry ,Receptors, G-Protein-Coupled ,03 medical and health sciences ,Mice ,0302 clinical medicine ,R5-920 ,FSLLRY-NH2 ,Tumor Cells, Cultured ,Medicine ,Animals ,Humans ,Receptor, PAR-2 ,Protease-activated receptor 2 ,Cell Proliferation ,Cervical cancer ,signal transducer and activator of transcription-3 ,Mice, Inbred BALB C ,business.industry ,protease-activated receptor-2 ,Biochemistry (medical) ,apoptosis ,Cell Biology ,General Medicine ,medicine.disease ,Pre-Clinical Research Reports ,Xenograft Model Antitumor Assays ,In vitro ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Apoptosis ,030220 oncology & carcinogenesis ,Cancer research ,STAT protein ,Female ,business ,Oligopeptides ,Signal Transduction - Abstract
Objective The present study explored how the inhibition of protease-activated receptor-2 (PAR-2) induced proliferation and apoptosis in cervical cancer in vitro and in vivo. Methods mRNA and protein expression of PAR2 and signal transducer and activator of transcription-3 (STAT-3) was determined by quantitative real-time PCR and western blotting. The proliferation and apoptosis of cervical cancer cells were assayed by the cell counting kit-8 kit, flow cytometry, and western blotting. The effects of PAR2 inhibition on cervical cancer were also examined in BALB/c nude mice in vivo. Results SLIGRL-NH2 (SL), a selective PAR-2 agonist, promoted proliferation and inhibited apoptosis of healthy cervical cancer cells and HeLa cells, while the PAR-2 antagonist FSLLRY-NH2 (FS) inhibited proliferation and led to apoptosis. SL also promoted the activation of STAT-3, while FS inhibited it and inhibited cancer growth in vivo. Conclusion FS inhibited cervical cancer by reducing proliferation and inducing apoptosis by interfering with STAT-3 signaling.
- Published
- 2019