Long non-coding RNA T-cell leukemia/lymphoma 6 serves as a sponge for miR-21 modulating the cell proliferation of retinoblastoma through PTEN
Sisi Tao1,*, Weidong Wang1,*, Pengfei Liu2, Hua Wang3, and Weirong Chen4
1Department of Science and Education, Changsha Hospital for Maternal & Child Health Care, Changsha 410007, Hunan, 2Department of Orthopedics, Shaoyang County People's Hospital, Shaoyang 422100, Hunan, 3Department of Ophthalmology, The First Affiliated Hospital of Human Normal University/Hunan Provincial People's Hospital, Changsha 410002, Hunan, 4Health Management Center, Changsha Hospital for Maternal & Child Health Care, Changsha 410007, Hunan, China
Received: August 11, 2018; Revised: December 28, 2018; Accepted: April 15, 2019
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Retinoblastoma (Rb) is one of the most common eye malignancies occur in childhood. The crucial roles of non-coding RNAs, particularly long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), have been widely reported in Rb progression. In the present study, we found the expression of lncRNA T-cell leukemia/lymphoma 6 (TCL6) was significantly downregulated in Rb tissues and cell lines. Knockdown of lncRNA TCL6 promoted cell proliferation while reduced cell apoptosis in Rb cells. Moreover, lncRNA TCL6 serves as a sponge for miR-21, a previously-reported oncogenic miRNA in Rb, by direct targeting to negatively regulated miR-21 expression, therefore modulating Rb proliferation through miR-21. TCL6 overexpression inhibited Rb cell proliferation while miR-21 overexpression exerted an opposing effect; the effect of TCL6 overexpression was partially attenuated by miR-21 overexpression. PTEN/PI3K/AKT signaling pathway was involved in lncRNA TCL6/miR-21 axis modulating Rb cell proliferation. Taken together, lncRNA TCL6 serves as a tumor suppressor by acting as a sponge for miR-21 to counteract miR-21-mediated PTEN repression.
Keywords: Cell proliferation; miRNA 21; Phosphate and tension homology deleted on chromsome ten (PTEN); Retinoblastoma