Breast cancer is a malignant tumor with the highest incidence in women of the world. CXCR4 and Skp2 are highly expressed in breast cancer cells and CXCR4 was positively correlated with Skp2 by interference or overexpression. The microRNA array was used to detect the differentially expressed spectrum of micro RNAs in breast cancer cells the changes of miR‐7‐5p after CXCR4 inhibitor (NT21MP) treatment to block the CXCR4/SDF‐1 pathway was founded. MiR‐7‐5p has been found to be correlated with Skp2 in various tumors in the literature, and Skp2 expression can be regulated by transfection with miR‐7‐5p mimics or inhibitors. The expression level of miR‐7‐5p was upregulated or downregulated after CXCR4 interference or overexpression. Combined with the correlation between CXCR4 and miR‐7‐5p in the chip results, CXCR4 may regulate Skp2 through miR‐7‐5p. Epithelial cells have the morphological characteristics of mesenchymal cells for some reason called epithelial–mesenchymal transformation (EMT). Transfection of miR‐7‐5p mimics into drug‐resistant cells reduced Skp2 levels, decreased the expression of Vimentin, Snail, and slug, and increased the expression of E‐cadherin. CXCR4 inhibitor (NT21MP) can reverse the EMT changes caused by miR‐7‐5p inhibitor. Similarly, in vivo results suggesting that CXCR4 inhibitors can reverse the EMT phenotype of drug‐resistant breast cancer cells through the CXCR4/miR‐7‐5p/Skp2 pathway. In summary, the CXCR4/miR‐7‐5p/Skp2 signaling pathway plays an important role in the progression of breast cancer. This study provides a theoretical basis for the treatment of breast cancer by targeting the CXCR4 pathway.

中文翻译：

---

源自vMIP-II的N端多肽通过CXCR4 / miR-7-5p / Skp2途径在人乳腺癌中发挥其抗肿瘤活性。

乳腺癌是世界上发病率最高的恶性肿瘤。CXCR4和Skp2在乳腺癌细胞中高表达，而CXCR4通过干扰或过表达与Skp2正相关。microRNA阵列用于检测乳腺癌细胞中micro RNA的差异表达谱，发现建立CXCR4抑制剂（NT21MP）处理以阻断CXCR4 / SDF-1途径后miR-7-5p的变化。在文献中发现，MiR-7-5p与各种肿瘤中的Skp2相关，并且可以通过转染miR-7-5p模拟物或抑制剂来调节Skp2的表达。在CXCR4干扰或过表达后，miR-7-5p的表达水平上调或下调。结合芯片结果中CXCR4和miR-7-5p之间的相关性，CXCR4可能通过miR-7-5p调节Skp2。由于某种原因，上皮细胞具有间充质细胞的形态特征，称为上皮-间质转化（EMT）。将miR-7-5p模拟物转染到耐药细胞中可降低Skp2水平，降低波形蛋白，蜗牛和的表达，并增加E-钙黏着蛋白的表达。CXCR4抑制剂（NT21MP）可以逆转由miR-7-5p抑制剂引起的EMT变化。同样，体内结果表明，CXCR4抑制剂可通过CXCR4 / miR-7-5p / Skp2途径逆转耐药乳腺癌细胞的EMT表型。总之，CXCR4 / miR-7-5p / Skp2信号通路在乳腺癌的进展中起着重要作用。该研究通过靶向CXCR4途径为乳腺癌的治疗提供了理论基础。