Research Paper Volume 12, Issue 1 pp 462—480
Down expression of lnc-BMP1-1 decreases that of Caveolin-1 is associated with the lung cancer susceptibility and cigarette smoking history
- 1 The State Key Lab of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical University, Xinzao, Guangzhou, China
- 2 The School of Public Health, The Institute of Environmental and Health of Dongguan Key Laboratory, Guangdong Medical University, Dongguan, China
- 3 The School of Public Health, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China
- 4 Department of English and American Studies, Faculty of Languages and Literatures, Ludwig Maximilian University (LMU), Munich, Germany
- 5 Shenzhen Longhua District Central Hospital, Shenzhen, Guangdong, China
- 6 The Fifth People’s Hospital of Dongguan, Dongguan, Guangdong, China
- 7 Department of Genetics, Medical College of Soochow University, Suzhou, China
- 8 Guangzhou Center for Disease Control and Prevention, Guangzhou, China
received: April 29, 2019 ; accepted: December 23, 2019 ; published: January 4, 2020 ;https://doi.org/10.18632/aging.102633
How to Cite
Copyright © 2020 Ling et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Lnc-BMP1-1 is a lncRNA transcribed from SFTPC (surfactant associated protein C), a lung tissue specific gene encoding pulmonary-associated surfactant protein C (SPC) that is solely secreted by alveolar typeⅡ epithelial cells, among which the ones with SFTPC+ might be transformed into lung adenocarcinoma cells. Caveolin-1 (Cav-1) is a candidate tumor suppressor gene and is vital for coping with oxidative stress induced by cigarette smoke. When comparing lung cancer tissues with their adjacent normal tissues, the expression of lnc-BMP1-1 were decreased, especially in patients with cigarette smoking history (P=0.027), and positively associated with the expression of Cav-1 (P<0.001). When comparing to A549 cells transfected with empty vector (A549-NC cells), the expression level of Cav-1 in A549 cells with over-expressed lnc-BMP1-1 (A549-BMP cells) was increased along with the decreased level of HDAC2 protein. The drug sensitivity of A549-BMP cells to Doxorubicin hydrochloride (DOX) was increased; the growth and migration capability of A549-BMP cells were inhibited along with the decreased protein level of Bcl-2 and DNMT3a; the growth of tumor in nude mice injected with A549-BMP cells were inhibited, too. Furthermore, the lnc-BMP1-1 and Cav-1 expression was also down-regulated in the human bronchial epithelial (16HBE) cells treated with cigarette smoke extract (CSE).