LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis

• Published in: BMC pulmonary medicine Vol. 21; no. 1; pp. 1 - 242
• Main Authors: Qian, Ye, Zhang, Yan, Ji, Haoming, Shen, Yucheng, Zheng, Liangfeng, Cheng, Shouliang, Lu, Xiaomin
• Format: Journal Article
• Language: English
• Published: London BioMed Central Ltd 19.07.2021; BioMed Central; BMC
• Subjects: Adenocarcinoma; Antibodies; Apoptosis; Binding sites; Breast cancer; Cell cycle; Cell growth; Cell migration; Cell proliferation; Cellular signal transduction; Development and progression; Genetic aspects; Health aspects; LINC01089; LUAD; Lung cancer; Membranes; miR-301b-3p; Morbidity; Non-coding RNA; Phenotypes; Pulmonology; RNA; STARD13; Variance analysis; Wound healing; China; United States > US; Japan; Germany
• ISSN: 1471-2466; 1471-2466
• DOI: 10.1186/s12890-021-01568-6

Abstract Background Lung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD. Methods The expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student’s t test or one-way analysis of variance. Results LINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells. Conclusion LINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.