淋巴结转移是导致宫颈癌患者死亡的主要原因。研究发现肿瘤相关巨噬细胞（TAM）表型重编程可促进肿瘤转移的发生。然而，TAM调控宫颈癌淋巴结转移的具体机制尚未阐明。我们预实验发现lncRNA-LNMICC在M2型TAM中显著高表达，抑制其表达可将M2型TAM逆转回M1型，进而抑制宫颈癌细胞转移及新生淋巴管生成。前期研究也证实LNMICC参与代谢重塑促进宫颈癌转移。由此我们推测：LNMICC可能通过介导TAM代谢应激变化使其表型重编程，进而促进宫颈癌发生淋巴结转移。因此，本项目拟进一步阐明LNMICC通过调控TAM精氨酸酶代谢及脂肪酸氧化应激变化，唤醒M2型TAM，从而激活宫颈癌细胞EMT及诱导淋巴管生成，促进宫颈癌淋巴结转移的机制。本研究将从lncRNA调控肿瘤相关巨噬细胞代谢应激的角度，揭示宫颈癌发生淋巴结转移的新机制，为宫颈癌患者的个体化精准治疗和预后改善提供潜在新靶标和新视角。

Lymph node metastasis is the primary cause of cervical cancer death. Numerous studies have shown that the reprogramming of macrophage phenotype can promote tumor metastasis.Its underlying molecular mechanisms, however, remain poorly understood. In our preliminary experiments, we observed that lncRNA-LNMICC was highly expressed in M2 TAM. And knockdown of LNMICC clearly triggered macrophage reprogramming from M2 phenotype towards an M1 phenotype and thus, significantly reduced metastatic ability of cervical cancer cells and lymphangiogenesis. Our previous studies also confirmed that lncRNA-LNMICC promoted lymph node metastasis of cervical cancer through taking part in cancer metabolism reprogramming. Therefore, our present project determines to further clarify the mechanisms of LNMICC in activating the EMT of cervical cancer cells and inducing lymphangiogenesis by regulating the metabolic of arginine and fatty acids in arousing M2 TAM. This project might reveal certain new mechanisms of lymph node metastasis from the perspective of cellular metabolic stress mediated by lncRNA in TAM, and provide novel biomarkers and strategies for achieving individualized precision treatment of cervical cancer, thus improving the overall prognosis of the disease.