Research Article

含有1的LEM结构域的升高可通过刺激PI3K/AKT通路预测NSCLC患者预后不良,引发NSCLC细胞的恶性干性和侵袭

卷 24, 期 3, 2024

发表于: 28 April, 2023

页: [366 - 378] 页: 13

弟呕挨: 10.2174/1566524023666230324135330

价格: $65

摘要

背景:非小细胞肺癌(NSCLC)是全球癌症相关死亡的主要原因。LEM结构域含有1 (LEMD1)功能已在几种癌症中发现,但在非小细胞肺癌中未发现。 目的:探讨LEMD1在非小细胞肺癌中的功能。 方法:获取66例NSCLC患者的组织,采用实时荧光定量PCR、免疫组化、Western blot检测LEMD1的表达。用Kaplan-Meier法估计NSCLC患者的总生存期。同时,采用Cell Counting kit - 8,5 - ethynyl -2 ' -脱氧尿苷分析、Transwell、Sphere formation assay和流式细胞术评估LEMD1的功能和机制。此外,通过建立异种移植肿瘤模型、苏木精-伊红染色和免疫组织化学分析来评估LEMD1在体内的功能。 结果:LEMD1在NSCLC组织中高表达,与肿瘤分化、TNM分期、患者淋巴结转移有关。高LEMD1的NSCLC患者的总生存率低于低LEMD1的患者。在功能上,干扰LEMD1抑制了非小细胞肺癌细胞的增殖、侵袭和干性特征。从机制上讲,LEMD1促进了NSCLC的恶性表型,而740 Y-P逆转了这种影响,提示LEMD1通过激活PI3K/AKT通路加重了NSCLC。此外,LEMD1敲低可抑制体内NSCLC的增殖。 结论:LEMD1通过激活PI3K/AKT通路加速非小细胞肺癌细胞增殖、侵袭和干细胞特性。

关键词: LEMD1, NSCLC, 增殖, PI3K/AKT, PCR, TNM 分期.

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