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Down expression of lnc-BMP1-1 decreases that of Caveolin-1 is associated with the lung cancer susceptibility and cigarette smoking history
Author(s) -
Xiaoxuan Ling,
Yinyan Li,
Fuman Qiu,
Xiaoxiao Lu,
Lei Yang,
Jinbin Chen,
Tiegang Li,
Di Wu,
Huali Xiong,
Wenpeng Su,
Dongsheng Huang,
Jiansong Chen,
Binyao Yang,
Hongjun Zhao,
Chenli Xie,
Yifeng Zhou,
Jiachun Lü
Publication year - 2020
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.102633
Subject(s) - a549 cell , lung cancer , cancer research , adenocarcinoma , caveolin 1 , lung , biology , transfection , chemistry , microbiology and biotechnology , cell culture , medicine , cancer , pathology , genetics
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).

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