Abstract

The role and mechanism of inflammation in breast cancer is unclear. This study aims to probe the relationship between inflammation and long non-coding RNAs (lncRNAs) and to stablish an inflammation-related competing endogenous RNA (ceRNA) network in breast cancer. Inflammation-related lncRNAs and target genes were screened based on the data from four single-cell RNA sequencing (scRNA-seq) studies and miRNAs were bioinformatically predicted according to ceRNA hypothesis. A series of in silico analyses were performed to construct an inflammation-related ceRNA network in breast cancer. Consequently, a total of seven inflammation-related lncRNAs were selected, after which LRRC75A-AS1 was identified as the most potential lncRNA in view of its expression and prognostic predictive value in breast cancer. Finally, an inflammation-related ceRNA network in breast cancer at the single cell level was established based on lncRNA LRRC75A-AS1, miR-3127-5p, miR-2114-3p, RPL36 and RPL27A mRNAs. Collectively, the lncRNA LRRC75A-AS1 and the LRRC75A-AS1-based on ceRNA network may exert crucial roles in modulating inflammation response during the initiation and progression of breast cancer.

Highlights

  • Breast cancer ranks the most common type of human cancer and is the leading cause of cancerrelated deaths in women all over the world (Sung et al, 2021)

  • These findings suggested that LRRC75A-AS1 might be the most potential inflammation-related long non-coding RNAs (lncRNAs) in breast cancer

  • Despite inflammation is present in breast cancer and may affect its outcome, the molecular mechanism of inflammation in breast carcinogenesis is still unknown

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Summary

Introduction

Breast cancer ranks the most common type of human cancer and is the leading cause of cancerrelated deaths in women all over the world (Sung et al, 2021). When Rudolph Virchow noted leucocytes in tumor tissues in 1863 and proposed the theory of “lymphoreticular infiltrate”, the origin of cancer at sites of inflammation came into researchers’ sight

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