Yunhu Pan1,2, Yitan Chen2, Debin Ma3, Zhiyu Ji2, Fangyu Cao2, Zhibin Chen2, Yunye Ning1, Chong Bai1. 1. a Department of Respiratory and Critical Care Medicine, Changhai Hospital , Second Military Medical University , Yangpu District , Shanghai , China. 2. b Department of Respiratory Medicine , No. 92 Hospital of Chinese People's Liberation Army , Yanping District, Nanping , Fujian , China. 3. c Department of Respiratory Medicine , General Hospital of Shenyang Military Area Command , Shenhe District, Shenyang , Liaoning , China.
Abstract
BACKGROUND: As one of the leading cause of cancer-related deaths in the worldwide, lung cancer needs to be understood better. Nowadays, increasing point mutations of specific oncogenes are biomarkers used to predict the therapeutic effect of targeted therapy and lung cancer has entered the age of individual treatment. At present, many relevant researchers have suggested that EGFR is a biomarker used to predict the therapeutic effect of targeted therapy. A large number of evidence indicates that EGFR/Akt pathway plays important role in cancer growth and metastasis. AIM OF THE STUDY: In this paper, we found EGFR was a target of miR-646. RESULTS: Overexpression of miR-646 not only downregulated EGFR/Akt pathway, but also inhibited lung cancer cell proliferation and metastasis. At the same time, miR-646 was a prognosis factor for overall survival. CONCLUSION: Our finding could provide new insights into the molecular therapeutic of lung cancer.
BACKGROUND: As one of the leading cause of cancer-related deaths in the worldwide, lung cancer needs to be understood better. Nowadays, increasing point mutations of specific oncogenes are biomarkers used to predict the therapeutic effect of targeted therapy and lung cancer has entered the age of individual treatment. At present, many relevant researchers have suggested that EGFR is a biomarker used to predict the therapeutic effect of targeted therapy. A large number of evidence indicates that EGFR/Akt pathway plays important role in cancer growth and metastasis. AIM OF THE STUDY: In this paper, we found EGFR was a target of miR-646. RESULTS: Overexpression of miR-646 not only downregulated EGFR/Akt pathway, but also inhibited lung cancer cell proliferation and metastasis. At the same time, miR-646 was a prognosis factor for overall survival. CONCLUSION: Our finding could provide new insights into the molecular therapeutic of lung cancer.
Authors: P Zhang; W M Tang; H Zhang; Y Q Li; Y Peng; J Wang; G N Liu; X T Huang; J J Zhao; G Li; A M Li; Y Bai; Y Chen; Y X Ren; G X Li; Y D Wang; S D Liu; J D Wang Journal: Br J Cancer Date: 2017-06-20 Impact factor: 7.640
Authors: Kai Ming Duan; Chao Fang; Si Qi Yang; Shu Ting Yang; Ji Dong Xiao; Huang Chang; Guo Xin Lin; Liang Bin Zhang; Ming Chao Peng; Zhao Qian Liu; Sai Ying Wang Journal: Front Genet Date: 2021-07-07 Impact factor: 4.599