目前的证据表明，miR-30家族在多种人类癌症中起到关键的作用（肿瘤抑制基因或致癌基因）。对microRNA（miRNA）表达谱和癌症基因图谱数据库（TCGA）的分析显示，miR-30c-1-3p和miR-30c-2-3p这两种被废弃链miRNA在癌组织中被下调表达，并且低表达与乳腺癌患者预后恶化密切相关。功能实验显示，miR-30c-1-3p和miR-30c-2-3p过表达显著抑制了癌细胞的侵袭能力，表明这两种miRNA在乳腺癌细胞中起到了肿瘤抑制基因的作用。值得注意的是，miRNA的废弃链参与是癌症研究中的一个新概念。进一步的分析显示，在乳腺癌细胞中，miR-30c-1-3p和miR-30c-2-3p有七个目标基因（TRIP13，CCNB1，RAD51，PSPH，CENPN，KPNA2和MXRA5）。七个基因在乳腺癌组织中的表达上调，并且预测了患者的不良预后。在这些基因中，我们关注了TRIP13，并研究了其在乳腺癌细胞中的功能意义。荧光素酶报告基因实验表明，这两种miRNA直接调控TRIP13。使用siRNA敲低TRIP13减弱了乳腺癌细胞的侵袭能力。使用特定的抑制剂对TRIP13进行失活可以防止乳腺癌细胞的恶性转化。探索被miRNA（包括废弃链）控制的分子网络将有助于在乳腺癌中鉴定诊断标记和治疗靶标分子。

Accumulating evidence suggests that the miR-30 family act as critical players (tumor-suppressor or oncogenic) in a wide range of human cancers. Analysis of microRNA (miRNA) expression signatures and The Cancer Genome Atlas (TCGA) database revealed that that two passenger strand miRNAs, miR-30c-1-3p and miR-30c-2-3p, were downregulated in cancer tissues, and their low expression was closely associated with worse prognosis in patients with BrCa. Functional assays showed that miR-30c-1-3p and miR-30c-2-3p overexpression significantly inhibited cancer cell aggressiveness, suggesting these two miRNAs acted as tumor-suppressors in BrCa cells. Notably, involvement of passenger strands of miRNAs is a new concept of cancer research. Further analyses showed that seven genes (TRIP13, CCNB1, RAD51, PSPH, CENPN, KPNA2, and MXRA5) were putative targets of miR-30c-1-3p and miR-30c-2-3p in BrCa cells. Expression of seven genes were upregulated in BrCa tissues and predicted a worse prognosis of the patients. Among these genes, we focused on TRIP13 and investigated the functional significance of this gene in BrCa cells. Luciferase reporter assays showed that TRIP13 was directly regulated by these two miRNAs. TRIP13 knockdown using siRNA attenuated BrCa cell aggressiveness. Inactivation of TRIP13 using a specific inhibitor prevented the malignant transformation of BrCa cells. Exploring the molecular networks controlled by miRNAs, including passenger strands, will facilitate the identification of diagnostic markers and therapeutic target molecules in BrCa.