Long intergenic noncoding RNA 00641 inhibits breast cancer cell proliferation, migration, and invasion by sponging miR‐194‐5p

Long noncoding RNAs have an essential role in the tumorigenesis of breast cancer (BC). Nonetheless, the consequences of long intergenic noncoding RNA 00641 (LINC00641) in BC remain unidentified. This study shows that LINC00641 expression level was decreased in BC tissues. LINC00641 expression level...

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Veröffentlicht in:Journal of cellular physiology 2020-03, Vol.235 (3), p.2668-2675
Hauptverfasser: Mao, Qixin, Lv, Minhao, Li, Lianfang, Sun, Yadong, Liu, Shanqing, Shen, Yan, Liu, Zhenzhen, Luo, Suxia
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Sprache:eng
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Zusammenfassung:Long noncoding RNAs have an essential role in the tumorigenesis of breast cancer (BC). Nonetheless, the consequences of long intergenic noncoding RNA 00641 (LINC00641) in BC remain unidentified. This study shows that LINC00641 expression level was decreased in BC tissues. LINC00641 expression level was negatively related to tumor size, lymph‐node metastasis, as well as clinical stage. LINC00641 overexpression inhibited cell proliferation, migration, and invasion but stimulated apoptosis in BC cells. LINC00641 overexpression also remarkably reduced BC growth and metastasis in vivo. LINC00641 acts as a competitive endogenous RNA to sponge miR‐194‐5p. miR‐194‐5p level was higher in BC tissues and cells compared with normal‐adjacent tissues and normal breast epithelial cell. miR‐194‐5p expression was negatively correlated with LINC00641 expression in BC tissues. miR‐194‐5p overexpression reversed the effects of LINC00641 on cell proliferation, cycle, apoptosis, migration, as well as invasion. In conclusion, LINC00641 inhibits BC cell proliferation, migration, as well as invasion by sponging miR‐194‐5p. Long intergenic noncoding RNA 00641 (LINC00641) is suggestively downregulated in breast cancer tissues as well as cell lines, while LINC00641 overexpression prevents breast cancer cell proliferation, migration, as well as invasion by sponging miR‐194‐5p.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.29170