Department of Thoracic Surgery, Binzhou People's Hospital, Binzhou, China.
Eur Rev Med Pharmacol Sci. 2018 Jan;22(2):443-449. doi: 10.26355/eurrev_201801_14193.
Lung cancer is highly heterogeneous and the 5-year survival rate is less than 15%. It is currently difficult to determine the heterogeneity of lung cancer and the underlying pathogenetic of metastasis. We aimed to investigate the effect of long non-coding RNA (lncRNA) TUC338 on the invasion of lung cancer by activating MAPK pathway and to understand the heterogeneity and metastasis mechanism of lung cancer.
The expression of lncRNA TUC338 in 42 samples of lung cancer and paracancerous tissues were accessed by RT-qPCR. The relationship between the expression of lncRNA and clinicopathological parameters was analyzed. After overexpressing and interfering with lncRNA TUC338, effects of lncRNA TUC338 on cell proliferation and invasion were determined by cell counting kit-8 (CCK8) and transwell assay. The protein expression was evaluated by Western blot.
Higher expression of TUC338 in lung cancer was observed in comparison with that in paracancerous tissues. The survival time of TUC338 was correlated with the expression of TUC338. Clinical data analysis revealed that the expression of TUC338 was correlated with the overall survival, tumor size and lymph node metastasis in patients, but not with age and gender. After interfering and overexpressing TUC338, it was found that the activity of lung cancer cells was decreased, as well as the invasion ability after interference with TUC338. After overexpression of TUC338, we found that lung cancer cell activity increased, as well as the invasion ability. By Western blot, we found that TUC338 can promote the development of lung cancer through regulating MAPK pathway.
TUC338 was overexpressed in lung cancer, and its expression may have a relationship to the prognosis of lung cancer. MAPK pathway was involved in the invasion of lung cancer regulated by TUC338.
肺癌具有高度异质性，5 年生存率低于 15%。目前，很难确定肺癌的异质性和转移的潜在发病机制。本研究旨在通过激活 MAPK 通路来研究长链非编码 RNA（lncRNA）TUC338 对肺癌侵袭的影响，并了解肺癌的异质性和转移机制。
通过 RT-qPCR 检测 42 例肺癌及癌旁组织中 lncRNA TUC338 的表达，分析 lncRNA 表达与临床病理参数的关系。过表达和干扰 lncRNA TUC338 后，通过细胞计数试剂盒-8（CCK8）和 Transwell 实验检测 lncRNA TUC338 对细胞增殖和侵袭的影响。通过 Western blot 评估蛋白表达。
与癌旁组织相比，肺癌组织中 TUC338 的表达较高。TUC338 的生存时间与 TUC338 的表达相关。临床数据分析显示，TUC338 的表达与患者的总生存期、肿瘤大小和淋巴结转移相关，而与年龄和性别无关。干扰和过表达 TUC338 后，发现肺癌细胞活性降低，干扰 TUC338 后侵袭能力也降低。过表达 TUC338 后，发现肺癌细胞活性增加，侵袭能力增强。通过 Western blot，我们发现 TUC338 可以通过调节 MAPK 通路促进肺癌的发生。
TUC338 在肺癌中过表达，其表达可能与肺癌的预后有关。MAPK 通路参与了 TUC338 调节的肺癌侵袭。
