All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

Role of lncRNA LUCAT1 in Promoting Radioresistance of Lung Cancer Cells through Sponging with miR-199a-5p

Author(s): Jing Cai and Yi Li*
Department of Pulmonary and Critical Care Medicine, Haining People???s Hospital, Jiaxing, Zhejiang 314400, China

Correspondence Address:
Yi Li, Department of Pulmonary and Critical Care Medicine, Haining People???s Hospital, Jiaxing, Zhejiang 314400, China, E-mail: jinsely3469@163.com


Radiotherapy is one of the most effective treatment strategies for lung cancer. However, radioresistance is a main limitation for lung cancer therapy. It is required to identify novel target to improve the radiotherapy efficacy of lung cancer. This study aimed to investigate the role of long non-coding ribonucleic acid lung cancer associated transcript 1 in the radioresistance of lung cancer. The correlation between lung cancer associated transcript 1 and patient survival was analyzed by using the cancer genome Atlas database. The expression of lung cancer associated transcript 1 in cells and lung cancer tissues was measured by real time polymerase chain reaction assay. Cell counting kit-8 assay and colony formation assay were used to determine the sensitivity of cells to ionizing radiation. Western blotting assay was performed to detect protein expressions and bioinformatic strategy was used to predict the target competing endogenous ribonucleic acids of lung cancer associated transcript 1. In the present study, we showed that long non-coding ribonucleic acid lung cancer associated transcript 1 is dramatically elevated in lung cancer cells and tissues, and high expression of lung cancer associated transcript 1 was negatively correlated with poor outcome in terms of overall survival. Moreover, knockdown of this long non-coding ribonucleic acid inhibited cell viability and increased cell apoptosis after irradiation, while lung cancer associated transcript 1 overexpression showed opposite effects. Mechanistically, knockdown of lung cancer associated transcript 1 elevated the activation of apoptosis factors B-cell lymphoma 2-associated X protein and cleaved-caspase 3. And lung cancer associated transcript 1 functions through binding with micro ribonucleic acid-199a-5p to regulate radiation response. In conclusion, we identified lung cancer associated transcript 1 as a factor promoting radioresistance in lung cancer, which provide novel target for cancer therapy.

Full-Text | PDF

 
 
Google scholar citation report
Citations : 66710

Indian Journal of Pharmaceutical Sciences received 66710 citations as per google scholar report