We attempted to investigate the relationship between hsa-let-7c and ANP32E, as well as their influence on the cells phenotype of lung adenocarcinoma. Expression of hsa-let-7c and prognostic values were assessed by bioinformatics analysis based on TCGA database. Quantitative real-time PCR and western blot was employed to measure relative expression of hsa-let-7c or ANP32E. The targeting relationship between let-7c and ANP32E was predicted by biological software and validated by dual luciferase reporter assay. With gene transfection technology, cell proliferation, invasion and migration were appraised by cell counting Kit-8, clone formation and Transwell assays. The results showed that hsa-let-7c was downregulated in lung adenocarcinoma. Downregulation of hsa-let-7c notably led to a poor survival. ANP32E was forecasted and confirmed as a directly target of hsa-let-7c, and was upregulated in lung adenocarcinoma. Furthermore, upregulation of ANP32E had a significant correlation with unsatisfactory survival. Meanwhile, the levels of ANP32E were negatively regulated by hsa-let-7c. Upregulation of hsa-let-7c remarkably suppressed the Calu-3 cell proliferation, invasion and migration, while ANP32E overexpression plasmids rescued the downtrend. Inversely, hsa-let-7c silencing in NCI-H209 cells presented the opposite outcomes. Collectively, hsa-let-7c shows an anti-tumor effect in lung adenocarcinoma by targeting ANP32E and is expected to be a potential therapeutic target for lung adenocarcinoma.

我们试图研究hsa-let-7c和ANP32E之间的关系，以及它们对肺腺癌细胞表型的影响。通过基于TCGA数据库的生物信息学分析评估hsa-let-7c的表达和预后价值。定量实时PCR和蛋白质印迹被用来测量hsa-let-7c或ANP32E的相对表达。let-7c和ANP32E之间的靶向关系已通过生物学软件进行了预测，并通过双重荧光素酶报告基因分析得以验证。利用基因转染技术，通过细胞计数Kit-8，克隆形成和Transwell分析评估了细胞的增殖，侵袭和迁移。结果表明，hsa-let-7c在肺腺癌中被下调。hsa-let-7c的下调明显导致存活率低下。ANP32E被预测并确认为hsa-let-7c的直接靶标，并且在肺腺癌中被上调。此外，ANP32E的上调与不良的生存率有显着的相关性。同时，hsa-let-7c负调节ANP32E的水平。hsa-let-7c的上调显着抑制了Calu-3细胞的增殖，侵袭和迁移，而ANP32E过表达质粒则挽救了下降趋势。相反，NCI-H209细胞中的hsa-let-7c沉默表现出相反的结果。总的来说，hsa-let-7c通过靶向ANP32E在肺腺癌中显示出抗肿瘤作用，并有望成为肺腺癌的潜在治疗靶标。ANP32E的上调与不良的生存率有显着的相关性。同时，hsa-let-7c负调节ANP32E的水平。hsa-let-7c的上调显着抑制了Calu-3细胞的增殖，侵袭和迁移，而ANP32E过表达质粒则挽救了下降趋势。相反，NCI-H209细胞中的hsa-let-7c沉默表现出相反的结果。总的来说，hsa-let-7c通过靶向ANP32E在肺腺癌中显示出抗肿瘤作用，并有望成为肺腺癌的潜在治疗靶标。ANP32E的上调与不良的生存率有显着的相关性。同时，hsa-let-7c负调节ANP32E的水平。hsa-let-7c的上调显着抑制了Calu-3细胞的增殖，侵袭和迁移，而ANP32E过表达质粒则挽救了下降趋势。相反，NCI-H209细胞中的hsa-let-7c沉默表现出相反的结果。总的来说，hsa-let-7c通过靶向ANP32E在肺腺癌中显示出抗肿瘤作用，并有望成为肺腺癌的潜在治疗靶标。NCI-H209细胞中的hsa-let-7c沉默表现出相反的结果。总的来说，hsa-let-7c通过靶向ANP32E在肺腺癌中显示出抗肿瘤作用，并有望成为肺腺癌的潜在治疗靶标。NCI-H209细胞中的hsa-let-7c沉默表现出相反的结果。总的来说，hsa-let-7c通过靶向ANP32E在肺腺癌中显示出抗肿瘤作用，并有望成为肺腺癌的潜在治疗靶标。