HIFU消融后残余肝癌易复发和转移是限制其广泛应用的主要障碍。在热消融等刺激下，癌细胞产生的tRF片段可抑制肿瘤恶性发展。课题组通过HIFU消融后残余肝癌细胞模型筛选出的tRFGln具有抑制残癌细胞增殖与侵袭的作用，并与HIFU消融术后肝癌患者的生存率负相关。而能与tRFGln的motif结合的CEBPα，具有促进肝癌细胞脂质代谢以抵抗凋亡的作用。另据报道称CEBPα是促进细胞内脂质代谢的关键酶—MAGL转录的主要转录因子，且MAGL的水平与肝癌患者的生存率呈负相关。因此，我们推测tRFGln通过负性调控CEBPα/MAGL轴介导的脂质代谢途径，是抑制HIFU消融后残肝癌细胞增殖和侵袭的主要机制。本项目将以CEBPα-MAGL-脂质代谢为轴线，探讨tRFGln对HIFU消融后残肝癌细胞增殖和侵袭能力的影响，为临床为进一步探索HIFU治疗肝癌的方式及HIFU消融后残余癌的治疗提供新的思路。

Recurrence and metastasis of Hepatocellular carcinoma (HCC) residual tumor after high intensive focused ultrasound (HIFU) have become the main obstacle of expanding the usage of HIFU. Under the stimulation of heat ablation, cancer cell derives stress-induced tRNA fragments (tRF) could restrain the progress of carcinoma. Our group screened out a tRFGln which could suppress proliferation and invasion of residual tumor cells from a HIFU ablation cell model. And this tRFGln was negatively corelated with survival time of HCC patients who received HIFU ablation. CEBPα, which could bind the motif of tRFGln, promotes lipolysis of HCC to against apoptosis and was reported the transcription factor of monoacylglycerol lipase a key rate-limiting enzyme of lipolysis the protein level which is negatively corelated with survival of HCC patients. Thus, we speculated tRFGln inhibits proliferation and invasion of HCC residual tumor after HIFU ablation by regulating CEBPα/MAGL axis. In this research, we discuss the impact of tRFGln to proliferation and invasion abilities of residual HCC cells after HIFU ablation along the axis of CEBPα-MAGL, to find a new path of managing residual HCC cells after HIFU ablation and to further improve the therapeutic effect.