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Table 5 CS‐regulated lncRNAs and their role in inflammation

From: The role of cigarette smoke-induced epigenetic alterations in inflammation

LncRNAs Changes by CS Functions on inflammation Mechanism Disease References Year
HOTAIR Upregulation [100, 101] Pro-inflammation Promote TNF-α production by activating NF-κB signaling
Promote the expression of protein kinase resource, TNF-α and IL-6
Promote the expression of IL‐6, IL‐1β, COX2, and TNF-α
Upregulated by pro-inflammatory cytokine IL-6
Sepsis
Keratinocyte injury
Atherosclerosis
Lung cancer
Wu et al. [201]
Liu and Zhang [203]
Liu et al. [204]
Liu et al. [101]
2016
2018
2019
2015
MALAT1 Upregulation [103] Pro-inflammation
Anti-inflammation
Activate p38 MAPK/NF-κB
Increase serum amyloid antigen 3
Upregulated by pro-inflammatory cytokine IL-6
Inhibit the DNA binding activity of NF-κB
Sepsis
Diabetes
Sepsis
N/A
Chen et al. [205]
Puthanveetil et al. [206]
Zhuang et al. [208]
Zhao et al. [207]
2018
2015
2017
2016
CCAT1 Upregulation [102] Pro-inflammation Trigger TNF-α, IFN-γ expression by targeting miR-185-3p, meanwhile upregulated by TNF-α Inflammatory bowel disease Ma et al. [209] 2019
  1. CCAT1 colon cancer-associated transcript-1, HOTAIR Hox transcript antisense intergenic RNA, MALAT1 metastasis associated in lung adenocarcinoma transcript 1