Open Access

ARTICLE

Long Noncoding RNA LINC02163 Accelerates Malignant Tumor Behaviors in Breast Cancer by Regulating the MicroRNA-511-3p/HMGA2 Axis

Chenglin Qin^*†, Linfang Jin^*‡, Jia Li^*§, Wenzhang Zha^†, Huiming Ding^†, Xiaorong Liu^*¶, Xun Zhu^*

* Department of Thyroid and Breast Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China
† Department of General Surgery, The Fourth Affiliated Hospital of Nantong Medical College, Yancheng City No. 1 People’s Hospital, Yancheng, Jiangsu, P.R. China
‡ Department of Pathology, Affiliated Hospital of Jiangnan University (Wuxi Fourth People’s Hospital), Wuxi, Jiangsu, P.R. China
§ Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, P.R. China
¶ Department of General Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, P.R. China

Oncology Research 2020, 28(5), 483-495. https://doi.org/10.3727/096504020X15928179818438

Abstract

Long intergenic nonprotein-coding RNA 02163 (LINC02163) has been reported to be upregulated and work as an oncogene in gastric cancer. The aims of the present study were to determine the expression profile and clinical value of LINC02163 in breast cancer. Additionally, the detailed functions of LINC02163 in breast cancer were explored, and relevant molecular events were elucidated. In this study, LINC02163 was upregulated in breast cancer, and its expression level was closely associated with tumor size, lymph node metastasis, and TNM stage. Patients with breast cancer presenting high LINC02163 expression exhibited shorter overall survival than those presenting low LINC02163 expression. Knockdown of LINC02163 resulted in a decrease in breast cancer cell proliferation, migration, and invasion and an increase in cell apoptosis in vitro. In addition, silencing of LINC02163 impeded breast cancer tumor growth in vivo. Mechanistic investigation revealed that LINC02163 served as a competing endogenous RNA for microRNA-511-3p (miR-511-3p) and consequently upregulated the expression of the high-mobility group A2 (HMGA2), a downstream target of miR-511-3p. Intriguingly, miR-511-3p inhibition and HMGA2 restoration counteracted the effects of LINC02163 deficiency on the malignant properties of breast cancer cells. LINC02163 exerts cancer-promoting effects during the initiation and progression of breast cancer via regulation of the miR-511-3p/HMGA2 axis. Our findings add to our understanding of the roles of the LINC02163/miR-511-3p/HMGA2 pathway as a regulator of breast cancer pathogenesis and may be useful in the development of lncRNA-directed cancer diagnosis, prognosis, and therapy.

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