LINC00467, Driven by Copy Number Amplification and DNA Demethylation, Is Associated with Oxidative Lipid Metabolism and Immune Infiltration in Breast Cancer

Overview

Journal Oxid Med Cell Longev

Publisher Wiley

Specialties Cell Biology
Endocrinology

Date 2021 Dec 27

PMID 34956437

Citations 13

Authors

Hao Bo

Wancong Zhang

Xiaoping Zhong

Jiasheng Chen

Yang Liu

Kit-Leong Cheong

Pengju Fan

Shijie Tang

Affiliations

Soon will be listed here.

Abstract

Breast cancer (BRCA) is a malignant tumor with a high incidence and poor prognosis in females. However, its pathogenesis remains unclear. In this study, based on bioinformatic analysis, we found that LINC00467 was highly expressed in BRCA and was associated with tumor metastasis and poor prognosis. The genomic and epigenetic analysis showed that LINC00467 may also be regulated by copy number amplification (CNA), chromatin openness, and DNA methylation. In vitro experiments showed that it could promote the proliferation, migration, and invasion of BRCA cells. Competitive endogenous RNA (ceRNA) regulatory network analysis and weighted gene coexpression network analysis (WGCNA) suggested that LINC00467 may play a role in signaling pathways of peroxisomal lipid metabolism, immunity, and others through microRNAs (miRNAs) targeting transforming growth factor beta 2 (TGFB2). In addition, copy number amplification and high expression of LINC00467 were associated with the low infiltration of CD8+ and CD4+ T cells. In conclusion, we found that LINC00467, driven by copy number amplification and DNA demethylation, may be a potential biomarker for the diagnosis and prognosis of BRCA and a tumor promoter acting as a potential therapeutic target for BRCA as well.

Citing Articles

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Somatic Copy Number Alterations in Colorectal Cancer Lead to a Differentially Expressed ceRNA Network (ceRNet).

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Long non‑coding RNAs, lipid metabolism and cancer (Review).

Zhang Z, Hou X, Cao X, Wang X Exp Ther Med. 2023; 26(4):470.

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