Chinese Journal of Clinical Oncology 2019;46(14):712-717
doi:10.3969/j.issn.1000-8179.2019.14.931
Expression and function of lncRNA BDNF-AS in breast cancer
Duoming WU 1 ; Li WU ; Xiaobin ZHANG
Affiliations
Keywords
breast cancer; long non-coding RNA (lncRNA); brain-derived neurotrophic factor (BDNF)
Country
China
Language
Chinese
Abstract
Objective: To determine expression of brain-derived neurotrophic factor antisense (BDNF-AS) long non-coding RNA (ln-cRNA) in breast cancer, and to investigate its effects on proliferation, apoptosis, migration and invasion. Methods: Between 2016 and 2018, samples from 88 cases of breast cancer were collected at the First Hospital of Lanzhou University. RT-qPCR was used to deter-mine expression of lncRNA BDNF-AS in breast cancer tissue and cells. A pcDNA3.1 plasmid was used to overexpress BDNF-AS in MDA-MB-231 cells. Cell viability was quantified using an MTT assay, proliferative capacity was determined using an EdU assay and a colori-metric assay was used to measure the Caspase-3 activity. Moreover, the protein levels of Bax, Bcl-2, MMP-9, E-cadherin, and BDNF were quantified by Western blot. Scratch and transwell assays were used to determine cell migration and invasion. Results: Lower ln-cRNA BDNF-AS expression was observed in breast cancer tissue and cells compared with normal paracancerous tissues (P<0.05), and with normal, HBL-100 breast cells (P<0.01). BDNF-AS expression negatively correlated with tumor-node-metastasis (TNM) stage (P<0.05) and lymphatic metastasis (P<0.05) of breast cancer. Overexpression of BDNF-AS with the pcDNA3.1 plasmid decreased viability of MDA-MB-231 cells (P<0.01), EdU-positive cells (P<0.01), and Caspase-3 activity (P<0.01). Additionally, Bcl-2, MMP-9, and BDNF ex-pression was downregulated (P<0.01), while Bax and E-cadherin expression was upregulated (P<0.01). Overexpression of BDNF-AS al-so inhibited cell healing and invasion which were determined by scratch assays (P<0.01). Conclusions: LncRNA BDNF-AS expression is downregulated in breast cancer, which inhibits breast cancer cell proliferation, migration, invasion, and promotes apoptosis.
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