LINC00052 promotes breast cancer cell progression and metastasis by sponging miR‑145‑5p to modulate TGFBR2 expression
- Menglu Dong
- Tao Xu
- Hanning Li
- Xingrui Li
Affiliations: Department of Thyroid and Breast Surgery, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
- Published online on: March 11, 2021 https://doi.org/10.3892/ol.2021.12629
Copyright: © Dong
et al. This is an open access article distributed under the
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Long non‑coding RNAs (lncRNAs) may participate in biological regulatory mechanisms of tumors. The aim of the present study was to uncover the molecular mechanism of the lncRNA LINC00052 in the tumorigenesis of breast cancer (BC). LINC00052 expression in BC tissues and cell lines was detected by reverse transcription‑quantitative PCR analysis. The Cell Counting Kit‑8, proliferation, Transwell and wound healing assays were employed to confirm the effect of LINC00052 on cell proliferation, migration and invasion. The cell localization of LINC00052 was estimated by cytoplasmic nuclear separation assay. Finally, the potential regulatory mechanism of LINC00052 in BC was detected by western blot analysis. The expression levels of LINC00052 were found to be significantly higher in BC tissues compared with those in the adjacent normal tissues. Downregulation of LINC00052 expression in vitro significantly suppressed the proliferation, migration and invasion of BC cells. LINC00052 was mainly expressed in the cytoplasm and was considered to bind with microRNA (miR)‑145‑5p based on various databases. Notably, the high expression levels of LINC00052 led to the low expression levels of miR‑145‑5p and high expression levels of TGF‑β receptor II (TGFBR2). In conclusion, the findings of the present study demonstrated that LINC00052 may sponge miR‑145‑5p to upregulate TGFBR2 expression in order to promote the proliferation and metastasis of BC cells. Therefore, LINC00052 may be an effective potential target for the diagnosis and treatment of BC.