Chen Wenshu, Zheng Guanying, Huang Jianyuan, Zhu Lihuan, Li Wujin, Guo Tianxing, Huang Yangyun, Pan Xiaojie
Department of Thoracic Surgery, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, No. 134 East Street, 350001, Fuzhou, China.
Department of Pulmonary and Critical Care Medicine, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, 350001, Fuzhou, China.
Cancer Cell Int. 2021 Feb 16;21(1):111. doi: 10.1186/s12935-021-01811-4.
Metastasis and disease refractoriness remain as major challenges for non-small cell lung cancer (NSCLC) treatment and understanding the underlying molecular mechanisms is of scientific and clinical value. Therefore, in this study, we aimed to explore the effects of circMED13L_012 on the proliferation, migration, invasion and drug-resistance of NSCLC tumor cells.
In this study, we utilized clinical samples and NSCLC cell lines to explore the association between circMED13L_012 expressions and tumor cell metastasis and chemo resistance. CCK8 and transwell assay were conducted to explore the impact of circMED13_012 on NSCLC tumor proliferation and migrative capabilities. Dual-luciferase reporter gene assay was conducted to validate the circMED13L_012 interaction network.
Our results demonstrated that circMED13L_012 exhibited significantly elevated average level in our clinical samples of NSCLC, compared with normal tissues. circMED13L_012 level was positively correlated with disease stage and metastatic status. Increased circMED13L_012 expression was associated with the enhanced migration, proliferation and chemo resistance of NSCLC cell lines. Further experiments indicated that circMED13L_012 promoted malignant behavior of NSCLC tumor cells by targeting MAPK8 through modulation miR-433-3p expression.
Our study for the first time demonstrated that circMED13L_012-miR-433-3p-MAPK8 axis played important role for NSCLC pathogenesis, which could be potential therapeutic target for the development of future NSCLC treatment.
转移和疾病难治性仍然是非小细胞肺癌（NSCLC）治疗的主要挑战，了解其潜在的分子机制具有科学和临床价值。因此，在本研究中，我们旨在探讨circMED13L_012对NSCLC肿瘤细胞增殖、迁移、侵袭和耐药性的影响。
在本研究中，我们利用临床样本和NSCLC细胞系来探讨circMED13L_012表达与肿瘤细胞转移和化疗耐药之间的关联。进行CCK8和Transwell实验以探究circMED13_012对NSCLC肿瘤增殖和迁移能力的影响。进行双荧光素酶报告基因实验以验证circMED13L_012的相互作用网络。
我们的结果表明，与正常组织相比，circMED13L_012在我们的NSCLC临床样本中表现出显著升高的平均水平。circMED13L_012水平与疾病分期和转移状态呈正相关。circMED13L_012表达的增加与NSCLC细胞系迁移、增殖和化疗耐药性的增强有关。进一步的实验表明，circMED13L_012通过调节miR-433-3p的表达靶向MAPK8来促进NSCLC肿瘤细胞的恶性行为。
我们的研究首次证明circMED13L_012-miR-433-3p-MAPK8轴在NSCLC发病机制中起重要作用，这可能是未来NSCLC治疗发展的潜在治疗靶点。
Zotero 插件
