Open Access

ARTICLE

Long noncoding RNA LINC02568 sequesters microRNA-874-3p to facilitate malignancy in breast cancer cells via cyclin E1 overexpression

YI DONG¹, LIANBO ZHANG², XIN GUAN³, TAO LIU¹, LIMIN ZHOU^1,*

1 Department of Second Breast Surgery, Jilin Cancer Hospital, Jilin, 130012, China
2 Department of Medical Insurance Guarantee Office, Jilin Cancer Hospital, Jilin, 130012, China
3 Department of Breast Surgery, The First Hospital of Jilin University, Jilin, 130061, China

* Corresponding Author: LIMIN ZHOU. Email:

Oncology Research 2021, 29(4), 291-303. https://doi.org/10.32604/or.2022.025172

Received 25 June 2022; Accepted 19 August 2022; Issue published 31 August 2022

Abstract

Increasing numbers of long noncoding RNAs (lncRNAs) are implicated in breast cancer oncogenicity. However, the contribution of LINC02568 toward breast cancer progression remains unclear and requires further investigation. Herein, we evaluated LINC02568 expression in breast cancer and clarified its effect on disease malignancy. We also investigated the mechanisms underlying the pro-oncogenic role of LINC02568. Consequently, LINC02568 was upregulated in breast cancer samples, with a notable association with worse overall survival. Functionally, depleted LINC02568 suppressed cell proliferation, colony formation, and metastasis, whereas LINC02568 overexpression exerted the opposite effects. Our mechanistic investigations suggested that LINC02568 was physically bound to and sequestered microRNA-874-3p (miR-874-3p). Furthermore, miR-874-3p mediated suppressive effects in breast cancer cells by targeting cyclin E1 (CCNE1). LINC02568 positively controlled CCNE1 expression by sequestering miR-874-3p. Rescue experiments revealed that increased miR-874-3p or decreased CCNE1 expression recovered cell growth and motility functions induced by LINC02568 in breast cancer cells. In conclusion, the tumor-promoting functions of LINC02568 in breast cancer cells were enhanced by sequestering miR-874-3p and consequently over-expressing CCNE1. Our data may facilitate the identification of novel therapeutic targets in clinical settings.

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Keywords

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