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Long Noncoding RNA TCONS_00068220 Promotes Breast Cancer Progression by Regulating Epithelial-Mesenchymal Transition Marker E-Cadherin

Xiao Liu, Xingsong Tian

(Department of Breast and Thyroid Surgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China (mainland))

Med Sci Monit 2021; 27:e929832

DOI: 10.12659/MSM.929832


BACKGROUND: Long noncoding RNAs (lncRNAs) play essential roles in the regulation of breast cancer development. We herein investigated the potential role of lncRNA TCONS_00068220 in breast cancer pathogenesis.
MATERIAL AND METHODS: The expression levels of TCONS_00068220 in breast cancer tissues were measured by qRT-PCR. Afterwards, TCONS_00068220 was (1) overexpressed in MCF-7 breast cancer cells, and (2) silenced in MDA-MB-231 cells. Then, CCK-8 and transwell assays were conducted to detect the impact of TCONS_00068220 on cell proliferation, migration, and invasion. The expression of the epithelial-mesenchymal transition (EMT) marker E-cadherin was detected by western blot assay after upregulation or downregulation of TCONS_00068220.
RESULTS: TCONS_00068220 was remarkably upregulated in breast cancer tissues compared with non-cancerous tissues. In addition, TCONS_00068220 level was significantly correlated with lymphatic metastasis, Ki67 index, clinical stage, and differentiation grade. All breast cancer cell lines displayed a higher expression level of TCONS_00068220 compared with the normal breast epithelial cell line MCF-10A. Furthermore, enhanced expression of TCONS_00068220 in MCF-7 cells promoted cell proliferation, migration, invasion, and EMT, whereas TCONS_00068220 knockdown in MDA-MB-231 cells led to the opposite results. E-cadherin was negatively regulated by TCONS_00068220 in both breast cancer tissues and cell lines. Finally, TCONS_00068220 regulated MCF-7 and MDA-MB-231 cell behaviors by downregulating E-cadherin.
CONCLUSIONS: TCONS_00068220 promotes breast cancer cell proliferation, migration, and invasion, while facilitating the process of EMT by interacting with E-cadherin and suppressing its expression. Therefore, it may potentially serve as an oncogene in breast cancer progression.

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