精准医学杂志 (Apr 2023)

EFFECT OF LONG NON-CODING RNA SMALL NUCLEOLAR RNA HOST GENE 1 ON MIGRATION, INVASION, AND EPITHELIAL-MESENCHYMAL TRANSITION OF BREAST CANCER CELLS AND ITS MECHANISM

  • DENG Lin, WU Qinglan, SONG Junying, GAO Xiao, XIAO Huanhuan, ZHANG Li, CAO Yi, HOU Lin

DOI
https://doi.org/10.13362/j.jpmed.202302014
Journal volume & issue
Vol. 38, no. 2
pp. 159 – 163

Abstract

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Objective To investigate the effect of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the migration, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells and its mechanism. Methods Breast cancer tissue samples and adjacent normal tissue samples were collected from 20 patients with breast cancer, and normal human breast epithelial cell MCF-10A and breast cancer cell lines MCF-7, BT-549, MDA-MB-231, and MDA-MB-468 were cultured. RT-qPCR was used to measure the expression levels of SNHG1 and miR-641 in tissue samples and cells. BT-549 cells were divided into groups A to D and were transfected with si-NC (group A), si-SNHG1 (group B), si-SNHG1+anti-miR-641-NC (group C), and si-SNHG1+anti-miR-641 (group D), respectively. RT-qPCR was used to measure the expression levels of SNHG1 and miR-641 in cells; Transwell assay was used to observe cell invasion and migration abilities; Western blot was used to measure the expression levels of the EMT-related proteins E-cadherin, N-cadherin, and Vimentin. BT-549 cells were divided into groups E to H and were co-transfected with SNHG1-WT and miR-641 mimics (group E), SNHG1-WT and miR-NC (group F), SNHG1-MUT and miR-641 mimics (group G), and SNHG1-MUT and miR-NC (group H), respectively, and dual-luciferase reporter assay was used to determine the interaction between SNHG1 and miR-641. Results SNHG1 was highly expressed in breast cancer tissue (t=4.81,P<0.05), while miR-641 was lowly expressed in breast cancer tissue (t=7.96,P<0.05). Compared with normal human breast epithelial cell line MCF-10A, the four breast cancer cell lines had a significantly upregulated expression of SNHG1 (t=8.11-10.79,P<0.05) and a significant reduction in the expression of miR-641 (t=9.16-11.17,P<0.05). Compared with group A, group B had significant reductions in the migration and invasion abilities of BT-549 cells and the protein expression le-vels of N-cadherin and Vimentin, as well as significant increases in the expression levels of N-cadherin and miR-641 (t=3.95-19.45,P<0.05). Compared with group C, group D had significant increases in the migration and invasion abilities of BT-549 cells and the protein expression levels of N-cadherin and Vimentin, as well as a significant reduction in the protein expression of E-cadherin (t=3.59-13.83,P<0.05). Dual-luciferase reporter assay showed that group E had a significantly lower luciferase activity than group F (t=8.37,P<0.05), and there was no significant difference in luciferase activity between groups G and H (P>0.05). Conclusion cSNHG1 is highly expressed in breast cancer tissue and cells, and downregulation of its expression can inhibit the migration, invasion, and EMT of breast cancer cells by targeting miR-641.

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