Xu Fengling, Lv Jiangfeng, Qin Shuang, Liu Lijuan, Ren Yuguo
Blood Transfusion Department, Jinan City People's Hospital, People's Hospital Affiliated to Shandong First Medical University, Jinan, 271100, China.
Department of Clinical Laboratory, Jinan City People's Hospital, People's Hospital Affiliated to Shandong First Medical University, Jinan, 271100, China.
Discov Oncol. 2025 Jun 14;16(1):1098. doi: 10.1007/s12672-025-02867-8.
TPM1 a member of TPM family and acts as a crucial role in a variety of tumors progression. However, the effect and mechanism of TPM1 on NSCLC need to be further explored. Here, effect and mechanism of TPM1 on NSCLC were revealed to provide new target for clinical therapy.
TPM1 expression in NSCLC tissues and normal tissues was analyzed using GEPIA online database. NSCLC cells were transfected with TPM1 overexpression plasmid. TPM1 mRNA expression of NSCLC cells was assessed by RT-qPCR. NSCLC cells proliferation and apoptosis were detected by CCK-8 and flow cytometry. Scratch healing and Transwell experiments were introduced to measure NSCLC cells migration and invasion. The effects of TPM1 overexpression on TPM1, YAP1 and EMT related proteins expression in NSCLC cells were detected by Western blot experiments. The interaction between TPM1 and YAP1 was analyzed by the HitPredict database and Co-IP assay.
TPM1 expression in NSCLC was decreased. High expression of TPM1 could inhibit NSCLC cells proliferation, migration and invasion and promote apoptosis. EMT marker E-Cadherin increased in TPM1 overexpression group, while Vimentin and N-Cadherin decreased. EMT process was inhibited by TPM1 overexpression. There is a mutual binding between TPM1 and YAP1, and TPM1 could down-regulate YAP1 expression. Overexpressed YAP1 could partly counteract the inhibition of NSCLC cells proliferation and metastasis induced by TPM1 overexpression.
TPM1 was down-regulated in NSCLC, and its overexpression inhibited NSCLC cells proliferation and metastasis, and this was achieved by regulating YAP1. TPM1 may become a new therapeutic target for NSCLC.
TPM1是TPM家族的成员之一，在多种肿瘤进展中发挥关键作用。然而，TPM1对非小细胞肺癌（NSCLC）的作用及机制仍需进一步探究。在此，揭示TPM1对NSCLC的作用及机制，为临床治疗提供新靶点。
使用GEPIA在线数据库分析NSCLC组织和正常组织中TPM1的表达。用TPM1过表达质粒转染NSCLC细胞。通过RT-qPCR评估NSCLC细胞中TPM1 mRNA的表达。采用CCK-8法和流式细胞术检测NSCLC细胞的增殖和凋亡。采用划痕愈合实验和Transwell实验检测NSCLC细胞的迁移和侵袭能力。通过蛋白质免疫印迹实验检测TPM1过表达对NSCLC细胞中TPM1、YAP1和上皮-间质转化（EMT）相关蛋白表达的影响。通过HitPredict数据库和免疫共沉淀实验分析TPM1与YAP1之间的相互作用。
NSCLC中TPM1表达降低。TPM1高表达可抑制NSCLC细胞的增殖、迁移和侵袭，并促进其凋亡。TPM1过表达组中EMT标志物E-钙黏蛋白增加，波形蛋白和N-钙黏蛋白减少。TPM1过表达抑制了EMT进程。TPM1与YAP1之间存在相互结合，且TPM1可下调YAP1的表达。过表达YAP1可部分抵消TPM1过表达对NSCLC细胞增殖和转移的抑制作用。
NSCLC中TPM1表达下调，其过表达可抑制NSCLC细胞的增殖和转移，这一作用是通过调节YAP1实现的。TPM1可能成为NSCLC的新治疗靶点。
