| Summary: | Huabo Jiang1 ,* Li Li2 ,* Jingjing Zhang,3 Zhong Wan,4 Yuanyuan Wang,5 Jingjing Hou,6 Yongsheng Yu1 1Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People’s Republic of China; 2Assisted Reproduction Technology Center, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 3Department of Plastic Surgery, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, People’s Republic of China; 4Urologic Medical Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China; 5Department of Health Medicine, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, People’s Republic of China; 6Department of Gastrointestinal Surgery, Institute of Gastrointestinal Oncology, Zhongshan Hospital of Xiamen University, Xiamen, Fujian, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jingjing Hou; Yongsheng Yu Email jjhou@xmu.edu.cn; yongshengyu@tongji.edu.cnObjective: EZH2 is the catalytic subunit of the polycomb repressive complex 2 (PRC2) and has been documented as an oncogene in breast cancer. The microRNA (miR)-101-3p can suppress breast cancer progression by targeting with EZH2. Syn-cal14.1a, a synthetic peptide derived from Californiconus californicus (Cal14.1a), can decrease the cell viability and activate the cell apoptosis in cancer. In this study, we explored whether the synergy of miR-101-3p mimic and syn-cal14.1a could inhibit the expression of EZH2. We also investigated this binding treatment’s effects on the suppression of breast cancer cells.Methods: MiR-101-3p mimic was transfected and syn-cal14.1a was added in SK-BR-3 and MCF-7 breast cancer cells. The expression of EZH2 protein level was determined. Then, cell proliferation, migration, invasion, and apoptosis were observed.Results: MiR-101-3p and syn-cal14.1a, when applied together, exerted a synergistic anti-EZH2 expression in breast cancer cells. The combination of miR-101-3p and syn-cal14.1a synergistically suppressed the EZH2-induced breast cancer cell migration, invasion, and proliferation. In parallel, this synergy treatment was able to promote the apoptosis of breast cancer cells. To our knowledge, this is the first report describing inhibition of EZH2 in human breast cancer cell lines by syn-cal14.1a.Conclusion: The anti-EZH2 roles of miR-101-3p and/or syn-cal14.1a could provide an effective therapeutic strategy in breast cancer. These data provide significant insights into molecular mechanisms of breast cancer and may have benefits in clinical therapeutics for breast cancer.Keywords: breast cancer, miR-101-3p, conotoxins, synthetic peptide, EZH2, synergism
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