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LINC02532 by Mediating miR-541-3p/HMGA1 Axis Exerts a Tumor Promoter in Breast cancer

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Abstract

The newly discovered LINC02532 is abnormally expressed in a variety of cancers and promotes cancer progression. The research proposed to discover the biological and molecular mechanisms of LINC02532 in breast cancer (BCa). In the resected BCa tissue samples and adjacent normal tissues, LINC02532, miR-541-3p, and High Mobility Group A1 (HMGA1) levels were determined. Cell function experiments were carried out on the premise of cell transfection with relevant plasmids. Based on that, the influence of LINC02532, miR-541-3p, and HMGA1 on MCF-7 cell activities (proliferation, migration, invasion, cell cycle, and apoptosis) was determined, as well as on EMT. Additionally, animal experiments were allowed to support cell experimental conclusions on LINC02532. Finally, the mechanistic network of LINC02532, miR-541-3p, and HMGA1 was identified. It was BCa tissues highly expressing LINC02532 and HMGA1, while lowly expressing miR-541-3p. Functionally, LINC02532 depletion repressed the activities and EMT process of MCF-7 cells. Silencing LINC02532 delayed tumor growth in mice. In terms of mechanism, LINC02532 mainly existed in the cytoplasm and could mediate HMGA1 expression by absorbing miR-541-3p. The findings offer new insights into the molecular mechanisms of LINC02532 in BCa and, more importantly, new strategies for the clinical treatment of BCa.

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Data is available from the corresponding author on request.

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Acknowledgements

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Funding

1. Shandong Provincial Natural Foundation (NO. ZR2020MH198). 2. Wu Jieping Medical Foundation Clinical Research Special Funding Fund (320.6750.2021-10-43).

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Correspondence to Rui Jiang or YuYang Li.

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All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. All subjects was approved by Shandong Provincial Hospital Affiliated to Shandong First Medical University. And The animal experiment research protocol was approved by the Ethics Committee of Shandong Provincial Hospital Affiliated to Shandong First Medical University and performed in accordance with the “Guidelines for the care and use of experimental animals.”

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12033_2023_995_MOESM1_ESM.tif

Supplementary Material 1: Fig. 1 Upregulation of LINC02532 promotes proliferation, migration, and invasion of MDA-MB-231 cells, and inhibits cell apoptosis pcDNA3.1-LINC02532 was transfected into MDA-MB-231 cells. RT-qPCR detection of the transfection of pcDNA3.1-LINC02532 (A), analysis results of proliferation (B-C), migration and invasion (D), apoptosis rate (E), and cell cycle (F). Data were expressed as mean ± SD, * P < 0.05

12033_2023_995_MOESM2_ESM.tif

Supplementary Material 2: Fig. 2 LINC02532 promotes proliferation, migration, and invasion and inhibits apoptosis of MDA-MB-231 cells by regulating miR-654-5p. si-LINC02532-1 and miR-654-5p inhibitor were co-transfected into MDA-MB-231 cells, RT-qPCR detection of the transfection of si-LINC02532-1 and miR-654-5p inhibitor (A), analysis results of proliferation (B-C), migration and invasion (D), apoptosis rate (E) and cell cycle (F). Data were expressed as mean ± SD, * P < 0.05

Supplementary Material 3

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Zhao, C., Li, X., Pan, X. et al. LINC02532 by Mediating miR-541-3p/HMGA1 Axis Exerts a Tumor Promoter in Breast cancer. Mol Biotechnol (2023). https://doi.org/10.1007/s12033-023-00995-6

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