MiR-101-3p and Syn-Cal14.1a Synergy in Suppressing EZH2-Induced Progression of Breast Cancer.
MiR-101-3p and Syn-Cal14.1a Synergy in Suppressing EZH2-Induced Progression of Breast Cancer.
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MiR-101-3p 和 Syn-Cal14.1a 协同抑制 EZH2 诱导的乳腺癌进展
DOI：
10.2147/ott.s264600
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发表时间：
2020
影响因子：
4
通讯作者：
Yu Y
中科院分区：
文献类型：
--
作者：
Jiang H;Li L;Zhang J;Wan Z;Wang Y;Hou J;Yu Y
目的 EZH2 是多梳抑制复合物 2 (PRC2) 的催化亚基，已被记录为乳腺癌的癌基因。 microRNA (miR)-101-3p 可以通过靶向 EZH2 来抑制乳腺癌进展。 Syn-cal14.1a 是一种源自加州 (Cal14.1a) 的合成肽，可降低癌症中的细胞活力并激活细胞凋亡。在本研究中，我们探讨了miR-101-3p模拟物和syn-cal14.1a的协同作用是否可以抑制EZH2的表达。我们还研究了这种结合治疗对抑制乳腺癌细胞的影响。方法转染MiR-101-3p模拟物并添加syn-cal14.1a到SK-BR-3和MCF-7乳腺癌细胞中。测定EZH2蛋白的表达水平。然后观察细胞增殖、迁移、侵袭和凋亡。结果 MiR-101-3p 和 syn-cal14.1a 一起应用时，在乳腺癌细胞中发挥协同抗 EZH2 表达。 miR-101-3p 和 syn-cal14.1a 的组合可协同抑制 EZH2 诱导的乳腺癌细胞迁移、侵袭和增殖。与此同时，这种协同治疗能够促进乳腺癌细胞的凋亡。据我们所知，这是第一份描述 syn-cal14.1a 在人类乳腺癌细胞系中抑制 EZH2 的报告。结论 miR-101-3p 和/或 syn-cal14.1a 的抗 EZH2 作用可以为乳腺癌提供有效的治疗策略。这些数据为乳腺癌的分子机制提供了重要的见解，并可能对乳腺癌的临床治疗有益。
Objective 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.