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. 2021 Mar 27;12(2):15–37. doi: 10.4331/wjbc.v12.i2.15

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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/

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Role of long non-coding RNAs in the pathophysiology of breast cancer. Long non-coding RNAs are reported to mediate pathophysiological developments such as metastasis as well as immune suppression within the tumor microenvironment. Metastasis-associated lung adenocarcinoma transcript 1 promotes growth and metastasis by controlling gene expression and post-translational modifications, invasion and migration by targeting tumor suppressor miRNA-129-5p, metastasis by transcriptionally regulating disruptor of telomeric silencing 1-like and promoting the interaction of hypoxia-inducible factor-2α. HOTAIR (HOX antisense intergenic RNA) increases invasiveness and metastasis by enhancing the expression of polycomb repressive complex 2 and altering the epigenome by histone H3 lysine 27 methylation, enhancing cell migration and invasiveness and inhibiting apoptosis through targeting high mobility AT-hook 2 via miRNA-20a-5p. MEG3 reduced angiogenesis by decreasing the expression of proangiogenic molecules as well as blocking Akt signaling. NKILA [nuclear factor-κappa beta (NF-κB) interacting lncRNA] negatively regulates tumor angiogenesis by decreasing the interleukin-dependent expression of vascular endothelial growth factor (VEGF)-A and VEGF-R through inhibiting NF-κB signaling and promotes antitumor immunity by inducing immune evasion of tumor cells via sensitizing T-cells through activation-induced cell death mechanism[57]. LINC00968 inhibits capillary formation by downregulating miRNA-423-5p mediated PROX1. LINC01133 promotes stem cell phenotypes by triggering miRNA-199a dependent FOXP2 signaling via modulation of Kruppel-like factor 4. Silencing of lncRNA-21 in tumor-associated macrophages induced apoptosis and reduced cell migration and invasion. LINK-A promotes antitumor immunity by inducing loss of antigenicity through PIP3 and inhibitory G-protein coupled receptor pathway as well as attenuating protein kinase A-dependent phosphorylation of E3 ubiquitin ligase TRIM71 and degradation of antigen peptide loading complex in triple-negative breast cancer. MALAT1: Metastasis-associated lung adenocarcinoma transcript 1; DOT1L: Disruptor of telomeric silencing 1-like; HIF: Hypoxia-inducible factor; HOTAIR: HOX antisense intergenic RNA; PRC2: Polycomb repressive complex 2; HMGA2: High mobility AT-hook 2; TNBC: Triple-negative breast cancer; IL: Interleukin; VEGF: Vascular endothelial growth factor.