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LncRNA LINC01772 promotes metastasis and EMT process in cervical cancer by sponging miR-3611 to relieve ZEB1

Tong MA1, §, Fafen WANG2, §, Xiaohui WANG1

1 Department of Obstetrics and Gynecology, First Hospital of Lanzhou University, Lanzhu, China
2 Department of Obstetrics and Gynecology, Huocheng County Maternal and Child Health Hospital, Yili Prefecture, China
§ These authors contributed equally to this work

* Address correspondence to: Xiaohui Wang,

BIOCELL 2019, 43(3), 191-198. https://doi.org/10.32604/biocell.2019.06989

Abstract

Cervical cancer (CC), has been identified as one of the most frequent malignant tumors all over the world, with high mortality in females. A growing number of investigations have confirmed that long noncoding RNAs (lncRNAs) play a crucial role in the progression of multiple cancers. Nonetheless, the biological function and regulatory mechanism of LINC01772 in CC haven’t been explored so far. In this study, LINC01772 expression was found to be upregulated in tissues and cells of CC. Knocking down LINC01772 suppressed CC cell proliferation, migration and epithelial-mesenchymal transition (EMT) process. Through molecular mechanism assays, LINC01772 was verified to be bound with miR-3611 and LINC01772 acted as a sponge for miR-3611. Zinc finger E-box binding homeobox 1 (ZEB1) was a downstream target gene of miR-3611. ZEB1 was negatively regulated by miR-3611 but positively regulated by LINC01772. Rescue assays confirmed that miR-3611 inhibitor or ZEB1 overexpression offset the inhibitive effect of LINC01772 depletion on cell proliferation, migration and EMT process in CC. In a word, our study validated that LINC01772 promoted cell metastasis and EMT process in CC by sponging miR-3611 to upregulate ZEB1 expression, indicating that LINC01772 could serve as a new therapeutic target for patients with CC.

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Cite This Article

MA, T., WANG, F., WANG, X. (2019). LncRNA LINC01772 promotes metastasis and EMT process in cervical cancer by sponging miR-3611 to relieve ZEB1. BIOCELL, 43(3), 191–198.



This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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