EMT在转移中的作用已获得广泛认可。但至今间质上皮转化（MET）在肿瘤中的作用却缺乏认识。Lin28A又叫多潜能因子，已知在胚胎干细胞具有重要作用。我们发现Lin28A是一种MET inducer，能促进细胞的上皮特征并抑制间质特性。我们用具有肺部微转移而无法形成转移灶的小鼠乳腺癌细胞系4TO7进行原位移植，发现lin28A可诱导肺部形成巨大转移灶，推测lin28A对乳腺癌的远端定值等后期转移相关。同时发现lin28A主要表达在上皮性乳腺癌细胞系中，符合其MET特性，并与干性增加相关。通过分子、细胞和动物水平，拟从两个方面阐述Lin28A调控乳腺癌转移的分子机制。一方面，Lin28A肿瘤调控TAM浸润可促进肿瘤肺转移，可能通过外泌体释放miR-125a和let7发挥作用。另一方面乳腺原位TAM浸润调控miR205，从而靶向VEGF-C信号并实现淋巴转移。以上作用可能均和MET转化密切相关。

EMT in cancer progression and metastasis has been widely studied in the last ten years. Mesenchymal–epithelial transition (MET) is suggested to participate in the process of metastatic tumor formation too. while the experimental data supportingthe role of MET in the process of carcinoma are still limited.Lin28A, an evolutionarily conserved RNA binding protein, is abundantly expressed in embryonic stem cells and is necessary for stem cell viability and pluripotency. Clinical data indicated that Lin28 overexpression is associated with advanced disease across multiple tumor types. Our results suggested that Lin28A promoted MET process in vitro, meanwhile, preliminarily indicated that Lin28A promoted the pulmonary metastasis of breast cancer via mammary fat pad graft. Histological examination found that high expression of Lin28A promoted TAM infiltration, which was indicative of high malignancy. The mechanism was initially determined that Lin28A up-regulatie the TAM and promote TAM M2 polarization to induce tumor invasion and pulmonary metastasis by directly binding to Let7 and miR-125a and inhibited its expression; moreover, Lin28A can upregulate PD-L1 both at primary and metastasis tumor. We will demonsrated that the molecular mechanism of Lin28A on Let7， miR-125a regulating . This work reveals a potential mechanism whereby , Lin28A, involves in MET process and TAM infiltration and impacts on the pulmonary metastasis of breast cancer. meanwhile, we show that the occurrence of lymphangiogennesis within mice breast cancers after mammary gland transplatation. Our results establish the of lymphangiogenesis in breast and identify lin28A-miR205-VEGFC as a molecuar link between tumor lymphangiogenesis and MET related metastasis.Nevertheless, this is a relatively new field of study and much remains to be established before the concept of TAM infiltration-induced lymphangiogenesis and lung metastasis are accepted as a viable anti-metastatic target. These observations will provide new targets for breast metastasis.