Melatonin has been recognized to slow breast cancer growth. The molecular mechanisms may involve long non-coding RNAs (lncRNAs). However, little is known on how melatonin affects lncRNA expression and function in breast cancer. We used microarrays to explore the expression profile of mRNAs and lncRNAs in melatonin-treated breast cancer cells. Kyoto encyclopedia of genes and genomes (KEGG) and Reactome pathways analysis were performed to identify the signaling pathways affected by altered expressed mRNAs after melatonin treatment. To explore the functions and mechanisms of the selected differentially expressed mRNA and lncRNA in breast cancer, we performed a series of experiments. We found that FK506-binding protein 3 (FKBP3) and lnc010561 were downregulated in melatonin-treated breast cancer cells. Knockdown of FKBP3 and lnc010561 inhibited breast cancer proliferation and invasion, and induced apoptosis. Also, lnc010561 and FKBP3 functioned as competing endogenous RNAs (ceRNAs) for miR-30. Our findings suggested that melatonin regulated breast cancer progression by the lnc010561/miR-30/FKBP3 axis. Melatonin may, therefore, function as an anticancer strategy for breast cancer.

褪黑激素已经被认为可以减缓乳腺癌的生长。分子机制可能涉及长的非编码RNA（lncRNA）。然而，关于褪黑激素如何影响乳腺癌中lncRNA表达和功能的知之甚少。我们使用微阵列来探索褪黑素治疗的乳腺癌细胞中mRNA和lncRNA的表达情况。进行了京都基因和基因组百科全书（KEGG）和Reactome途径分析，以确定褪黑素处理后受表达mRNA改变影响的信号传导途径。为了探索乳腺癌中差异表达的mRNA和lncRNA的功能和机制，我们进行了一系列实验。我们发现在褪黑素治疗的乳腺癌细胞中，FK506结合蛋白3（FKBP3）和lnc010561被下调。抑制FKBP3和lnc010561抑制乳腺癌的增殖和侵袭，并诱导细胞凋亡。另外，lnc010561和FKBP3充当miR-30的竞争内源RNA（ceRNA）。我们的发现表明褪黑激素通过lnc010561 / miR-30 / FKBP3轴调节乳腺癌的进展。因此，褪黑激素可以作为乳腺癌的抗癌策略。