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Research Article

Circular RNA Hsa_Circ_0072995 Promotes Breast Cancer Cell Migration and Invasion Through Sponge for Mir-30c-2-3p

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Pages 1229-1242 | Received 02 Jan 2018, Accepted 22 May 2018, Published online: 05 Sep 2018
 

Abstract

Aim: To study the role of hsa_circ_0072995 in regulating the invasion and migration of breast cancer cells. Materials & methods: Hsa_circ_0072995 expression was confirmed by quantitative real-time PCR; evaluating the migration and invasion of breast cancer cells through transwell assay; predicating circRNA/microRNAs interaction using the miRanda and RNAhybrid software; identifying the relationship between hsa_circ_0072995 and miR-30c-2-3p by luciferase activity assay; detecting the location of hsa_circ_0072995 by Fluorescence in situ hybridization assay. Results: Hsa_circ_0072995 was significantly upregulated in MDA-MB-231 cells compared with MCF-7 cells. Hsa_circ_0072995 regulated the invasion and migration of breast cancer cells. Hsa_circ_0072995 existed in the nucleus and cytoplasm, and the proportion of the two was roughly equal. Hsa_circ_0072995 bound to miR-30c-2-3p. Overexpression of miR-30c-2-3p inhibited breast cancer cells migration and invasion. Low expression of miR-30c-2-3p was correlated with poor overall survival by The Cancer Genome Atlas database. Conclusion: Hsa_circ_0072995 may be a novel biomarker for breast cancer, and may function in metastasis of breast cancer.

Financial & competing interests disclosure

This research was supported by the National Key Research and Development Program of China (No. 2016YFC0905900). Natural Science Foundation of Jiangsu Province (No. BK20151579). National Natural Science Foundation of China (grant number 81702613). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This research was supported by the National Key Research and Development Program of China (No. 2016YFC0905900). Natural Science Foundation of Jiangsu Province (No. BK20151579). National Natural Science Foundation of China (grant number 81702613). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.

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