人参皂苷Rg3抑制非小细胞肺癌细胞重编程的机制研究

Mechanism Research of Ginsenoside Rg3 Inhibiting Reprogramming of Non-Small Cell Lung Cancer Cells

非小细胞肺癌(NSCLC)作为一种常见的肺部恶性肿瘤,其全球发病率和死亡率仍处于较高水平。尽管传统疗法在局部晚期和转移性NSCLC的治疗方面取得了一定进展,但鉴于肿瘤细胞具有免疫逃逸特性,治疗效果尚不理想。研究发现肿瘤细胞重编程是导致免疫逃逸的重要因素。人参皂苷Rg3作为人参的有效活性成分,是一种具有不同结构的天然小分子化合物,其主要作用为辅助抗肿瘤。通过抑制NSCLC细胞的重编程,人参皂苷Rg3的主要抗肿瘤免疫逃逸机制包括降低肿瘤细胞免疫检查点PD-L1的表达、抑制上皮间质转化(EMT)以及肿瘤细胞干性。本文将从上述三个方面对人参皂苷Rg3抑制非小细胞肺癌细胞重编程的机制展开论述。

Non small cell lung cancer(NSCLC)is the most common lung cancer,with a high incidence rate and mortality worldwide.Although traditional treatment methods have made progress in treatment of locally advanced and metastatic NSCLC,curative effect is still unsatisfactory due to immune escape of tumor cells.Research has found tumor cell reprogramming is an important factor of immune escape.Ginsenoside Rg3,as an effective active ingredient of ginseng,is a natural small molecule compound with different structures,with effect of auxiliary anti-tumor.Main mechanisms of ginsenoside Rg3 inhibitting tumor cell immune escape by inhibiting NSCLC cell reprogramming include reducing expression of tumor cell immune checkpoint PD-L1,inhibiting epithelial mesenchymal transition(EMT)and tumor cell stemness.The paper discusses mechanism of ginsenoside Rg3 inhibiting reprogramming in non-small cell lung cancer cells from above three aspects.