Research Papers:

This article has been retracted. Retraction in: Oncotarget. 2023; 14:363-363.

LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis

Dongmei Han, Jianfeng Wang and Guanghui Cheng _

PDF  |  HTML  |  How to cite

Oncotarget. 2018; 9:2395-2409. https://doi.org/10.18632/oncotarget.23416

Metrics: PDF 2190 views  |   HTML 2857 views  |   ?  


Dongmei Han1, Jianfeng Wang1 and Guanghui Cheng1

1Department of Radiation Oncology, China-Japan Union Hospital of Jilin University, Changchun 130033, China

Correspondence to:

Guanghui Cheng, email: [email protected]

Keywords: lncRNA NEAT1; radio-resistance; cervical cancer; miR-193b-3p/CCND1 axis

Received: September 19, 2017    Accepted: December 04, 2017    Published: December 18, 2017


LncRNAs have become a hot topic in various cancer-related researches. Radio-resistance is a great threat for cancer therapy. However, how lncRNAs affect the radio-resistance in cervical cancer is masked. As for our paper, it was discovered that NEAT1 was highly expressed in cervical cancer tissues and non-sensitive tissues as well as radio-resistant cell lines. And the overexpression of NEAT1 accelerated proliferation, while the knockdown of NEAT1 had the opposite result. The effect of NEAT1 on cell proliferation was dependent on the dose of ionizing radiation. And the silence of NEAT1 also caused cell cycle arrest in G0/G1 phase, and triggered more apoptosis, indicating the oncogenic role of NEAT1 in cervical cancer. Next, mechanistic assays affirmed that NEAT1 could function as a ceRNA to regulate cyclin D1 through sponging miR-193b-3p in cervical cancer. Rescue assays were employed to validate that miR-193b-3p and cyclin D1 could inhibit NEAT1-mediated suppressive effect on proliferation, and its stimulative effect on cell cycle arrest and apoptosis. In general, this article disclosed that NEAT1 could facilitate the radio-resistance of cervical cancer via competitively binding miR-193b-3p to up-regulate the expression of cyclin D1.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 23416