Functional role and mechanism of lncRNA LOC728228 in malignant 16HBE cells transformed by anti‐benzopyrene‐trans‐7, 8‐dihydrodiol‐9, 10‐epoxide. Issue 1 (27th March 2015)

• Record Type: Journal Article
• Authors: Hu, Gongcheng; Yang, Ti; Zheng, Jingli; Dai, Jiabing; Nan, Aruo; Lai, Yandong; Zhang, Yajie; Yang, Chengfeng; Jiang, Yiguo; Schabath, Matthew B.; DiGiovanni, John
• Is Part Of: Molecular carcinogenesis. Volume 54:Issue 1(2015:Jan.)
• Page Start: E192
• Page End: E204
• Publication Date: 2015-03-27
• Subjects: Carcinogenesis -- Molecular aspects -- Periodicals; 616.994071
• DOI: 10.1002/mc.22314
• Languages: English
• ISSNs: 0899-1987

Abstract

<abstract abstract-type="main" xml:lang="en"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mc22314-sec-0001" sec-type="section"> <p>Lung cancer is a major health problem, and is considered one of the deadliest cancers in humans. It is refractory to current treatments, and the mechanisms of lung cancer are unknown. Long noncoding RNAs (lncRNAs) are involved in various biological processes and human diseases. However, the exact functional roles and mechanisms of lncRNAs are largely unclear. In this study, we attempted to identify lung‐cancer‐related lncRNAs. We found changes in lncRNA expression in the anti‐benzo(a) pyrene‐7, 8‐diol‐9, 10‐epoxide (anti‐BPDE)‐transformed human bronchial epithelial cell line (16HBE‐T cells) using microarrays and qRT–PCR. Of these lncRNAs, LOC728228 was upregulated relative to its expression in control untransformed16HBE (16HBE‐N) cells. LOC728228 knockdown inhibited cell proliferation, caused G0/G1‐phase cell‐cycle arrest, reduced cellular migration, suppressed colony formation in vitro, and inhibited tumor growth in a nude mouse xenograft model. LOC728228 knockdown also suppressed cyclin D1 expression, and the depletion of cyclin D1 induced G0/G1‐phase cell‐cycle arrest and inhibited cell proliferation, thus influencing the malignant potential of cancer cells. In summary, our results suggest that lncRNA LOC728228 has an oncogene‐like function and plays a vital role in human lung cancer. © 2015 Wiley Periodicals, Inc.</p> </sec> </abstract>