Yanli Yuan1, Xiaolei Zhou1, Yan Kang2, Hongping Kuang1, Qiang Peng1, Bo Zhang1, Xinxin Liu1, Manlin Zhang3. 1. Department of Respiratory and Critical Care Ward 3, Henan Provincial Chest Hospital, Zhengzhou, Henan, China. 2. Department Two of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China. 3. Department of Respiratory and Critical Care Ward 3, Henan Provincial Chest Hospital, Zhengzhou, Henan, China. Electronic address: yylxkyy@126.com.
Abstract
BACKGROUND: Increasing biomolecules have been found to be involved in the lung cancer development. This study will perform the function and mechanism analyses of a novel circular RNA copper chaperone for superoxide dismutase (circ-CCS) in lung cancer. METHODS: Circ-CCS, microRNA-383 (miR-383) and E2F transcription factor 7 (E2F7) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was detected using Cell Counting Kit-8 (CCK-8). Clonal ability was measured by colony formation assay. Cell apoptosis was determined via flow cytometry. Cell migration and invasion were assessed by transwell assay. Detection of protein was completed using western blot. Xenograft assay was used for the functional analysis of circ-CCS in vivo. The binding between targets was proved by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. E2F7 protein level was also examined by Immunohistochemistry (IHC) analysis in human tissues. RESULTS: Circ-CCS was upregulated in lung cancer and could predict poor prognosis. Downregulation of circ-CCS inhibited lung cancer cell growth and metastasis while promoted apoptosis in vitro, and suppressed tumorigenesis of lung cancer in vivo. Circ-CCS had sponge effect on miR-383 and the function of si-circ-CCS was achieved by upregulating miR-383. E2F7 was a target gene of miR-383 and its downregulation was responsible for the anti-cancerous role of miR-383 in lung cancer. Circ-CCS could elevate E2F7 expression via interacting with miR-383. CONCLUSION: Circ-CCS was shown to facilitate lung cancer progression via the miR-383/E2F7 axis, exhibiting the pivotal value of circ-CCS in diagnosis and treatment of lung cancer.
BACKGROUND: Increasing biomolecules have been found to be involved in the lung cancer development. This study will perform the function and mechanism analyses of a novel circular RNA copper chaperone for superoxide dismutase (circ-CCS) in lung cancer. METHODS: Circ-CCS, microRNA-383 (miR-383) and E2F transcription factor 7 (E2F7) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was detected using Cell Counting Kit-8 (CCK-8). Clonal ability was measured by colony formation assay. Cell apoptosis was determined via flow cytometry. Cell migration and invasion were assessed by transwell assay. Detection of protein was completed using western blot. Xenograft assay was used for the functional analysis of circ-CCS in vivo. The binding between targets was proved by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. E2F7 protein level was also examined by Immunohistochemistry (IHC) analysis in human tissues. RESULTS: Circ-CCS was upregulated in lung cancer and could predict poor prognosis. Downregulation of circ-CCS inhibited lung cancer cell growth and metastasis while promoted apoptosis in vitro, and suppressed tumorigenesis of lung cancer in vivo. Circ-CCS had sponge effect on miR-383 and the function of si-circ-CCS was achieved by upregulating miR-383. E2F7 was a target gene of miR-383 and its downregulation was responsible for the anti-cancerous role of miR-383 in lung cancer. Circ-CCS could elevate E2F7 expression via interacting with miR-383. CONCLUSION: Circ-CCS was shown to facilitate lung cancer progression via the miR-383/E2F7 axis, exhibiting the pivotal value of circ-CCS in diagnosis and treatment of lung cancer.