Baykara Onur, Dalay Nejat, Kaynak Kamil, Buyru Nur
Department of Medical Biology, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul, Turkey.
Istanbul University Oncology Institute, Istanbul, Turkey.
Cancer Med. 2016 Oct;5(10):2873-2878. doi: 10.1002/cam4.847. Epub 2016 Sep 20.
Despite therapeutic advances, lung cancer remains one of the most common causes of cancer-related deaths worldwide. The ZNF703 gene has been identified as the driver of the 8p11-12 region and its amplification or overexpression has been associated with several types of cancers. It has also been shown that ZNF703 overexpression can activate the Akt/mTOR signaling pathway. The aim of our study was to investigate the role of the ZNF703 gene in association with Akt/mTOR activation in non-small cell lung cancer (NSCLC). Expression levels in tumors and matched noncancerous tissue samples from 47 patients were analyzed by qRT-PCR and the Akt phosphorylation levels were investigated by Western blotting. Our results show that ZNF703 is up-regulated in 63.4% of NSCLC tumor samples. Althogh the correlation did not reach a statistically significant level Akt phosphorylation was increased in tumor tissues expressing high levels of ZNF703. The role of the ZNF703 gene has not been investigated in NSCLC. Our data show that ZNF703 may contribute to tumor development in NSCLC by activating the Akt/mTOR pathway.
尽管治疗取得了进展，但肺癌仍然是全球癌症相关死亡的最常见原因之一。ZNF703基因已被确定为8p11 - 12区域的驱动基因，其扩增或过表达与多种癌症类型相关。研究还表明，ZNF703过表达可激活Akt/mTOR信号通路。我们研究的目的是探讨ZNF703基因在非小细胞肺癌（NSCLC）中与Akt/mTOR激活相关的作用。通过qRT-PCR分析了47例患者肿瘤及配对的非癌组织样本中的表达水平，并通过蛋白质印迹法研究了Akt磷酸化水平。我们的结果显示，63.4%的NSCLC肿瘤样本中ZNF703上调。尽管相关性未达到统计学显著水平，但在表达高水平ZNF703的肿瘤组织中Akt磷酸化增加。ZNF703基因在NSCLC中的作用尚未得到研究。我们的数据表明，ZNF703可能通过激活Akt/mTOR通路促进NSCLC的肿瘤发展。
