Long non‑coding RNA, CHRF, predicts poor prognosis of lung adenocarcinoma and promotes cell proliferation and migration

Xie, Xiaowei; Zhao, Wei; Pang, Jinglin; Xiong, Xiaomiao; Wang, Haiyan; Ma, Lingyun

doi:10.3892/ol.2018.9425

Cited by 3 publications

(4 citation statements)

References 31 publications

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“…LncRNA cardiac hypertrophy-related factor (CHRF) functions as an oncogene, promoting migration and invasion in various tumor types [ 167 ]. In a silica-induced pulmonary fibrosis mouse model, CHRF activates inflammatory and fibrotic pathways via the miR-489/MyD88 and miR-489/SMAD3 axes, with SMAD3 being an adaptor in receptor-regulated signaling [ 108 , 168 ].…”

Section: Lncrnas That Modulate Macrophage Nf-κb Activity In Cancermentioning

confidence: 99%

Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases

Shin,

Park,

Shin

et al. 2024

IJMS

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Over the past century, molecular biology’s focus has transitioned from proteins to DNA, and now to RNA. Once considered merely a genetic information carrier, RNA is now recognized as both a vital element in early cellular life and a regulator in complex organisms. Long noncoding RNAs (lncRNAs), which are over 200 bases long but do not code for proteins, play roles in gene expression regulation and signal transduction by inducing epigenetic changes or interacting with various proteins and RNAs. These interactions exhibit a range of functions in various cell types, including macrophages. Notably, some macrophage lncRNAs influence the activation of NF-κB, a crucial transcription factor governing immune and inflammatory responses. Macrophage NF-κB is instrumental in the progression of various pathological conditions including sepsis, atherosclerosis, cancer, autoimmune disorders, and hypersensitivity. It orchestrates gene expression related to immune responses, inflammation, cell survival, and proliferation. Consequently, its malfunction is a key contributor to the onset and development of these diseases. This review aims to summarize the function of lncRNAs in regulating NF-κB activity in macrophage activation and inflammation, with a particular emphasis on their relevance to human diseases and their potential as therapeutic targets. The insights gained from studies on macrophage lncRNAs, as discussed in this review, could provide valuable knowledge for the development of treatments for various pathological conditions involving macrophages.

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Section: Lncrnas That Modulate Macrophage Nf-κb Activity In Cancermentioning

confidence: 99%

Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases

Shin,

Park,

Shin

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…LncRNA cardiac hypertrophy-related factor (CHRF) functions as an oncogene, promoting migration and invasion in various tumor types [167]. In a silica-induced pulmonary fibrosis mouse model, CHRF activates inflammatory and fibrotic pathways via the miR-489/MyD88 and miR-489/SMAD3 axes, with SMAD3 being an adaptor in receptorregulated signaling [108,168].…”

Section: Lncrnas That Modulate Macrophage Nf-κb Activity In Cancermentioning

confidence: 99%

LncRNAs Affecting NF-κB-Mediated Macrophage Inflammation Are Potential Therapeutic Targets in Human Diseases

Shin,

Park,

Shin

et al. 2024

Preprint

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The studies regarding macrophage lncRNAs described in this review can help provide valuable information for developing treatments for various pathological conditions involving macrophages. Over the past century, molecular biology's focus has transitioned from proteins to DNA, and now to RNA. Once considered merely a genetic information carrier, RNA is now recognized as both a vital element in early cellular life and a regulator in complex organisms. Long noncoding RNAs (lncRNAs), which are over 200 bases long but do not code for proteins, play roles in gene expression regulation and signal transduction by inducing epigenetic changes or interacting with various proteins and RNAs. These interactions exhibit a range of functions in various cell types including macrophages. Notably, some macrophage lncRNAs influence the activation of NF-κB, a crucial transcription factor governing immune and inflammatory responses. Macrophage NF-κB is instrumental in the progression of various pathological conditions including sepsis, atherosclerosis, cancer, autoimmune disorders, and hypersensitivity. It orchestrates gene expression related to immune responses, inflammation, cell survival, and proliferation. Consequently, its malfunction is a key contributor to the onset and development of these diseases. This review summarizes the role of lncRNAs that regulate NF-κB in macrophage activation and inflammation, especially focusing on their implications in human diseases and their potential as therapeutic targets

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“…CHRF, a newly recognized lncRNA, is a central regulator in diseases. [18][19][20] But its function in myocardial I/R injury is unclear. To investigate the CHRF expression in myocardial I/R injury, an in vivo model of myocardial I/R injury was established.…”

Section: Inhibition Of Chrf Relieved Myocardial I/r Injury In Vivomentioning

confidence: 99%

“…[ 17 ] CHRF results in poor prognosis and aggravates cell proliferation and migration in lung adenocarcinoma. [ 18 ] Furthermore, the inhibition of CHRF upregulates miRNA‐221 to protect against lipopolysaccharide‐induced injury in H9C2 cells. [ 19 ] LncRNA CHRF inhibits miR‐489 to regulate cardiac hypertrophy progression.…”

Section: Introductionmentioning

confidence: 99%

LncRNA CHRF aggravates myocardial ischemia/reperfusion injury by enhancing autophagy via modulation of the miR‐182‐5p/ATG7 pathway

Yipeng

Zheng

et al. 2021

J Biochem & Molecular Tox

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Myocardial ischemia/reperfusion (I/R) injury is a very frequent cardiovascular disease and one of the leading causes of death. Abundant evidence has shown that long noncoding RNAs (lncRNAs) are crucial players in myocardial I/R injury. LncRNA cardiac hypertrophy‐related factor (CHRF) has been revealed as an important modulator in cardiac disease. However, the function of CHRF in myocardial I/R injury is unclear. In our current work, we found that the expression of CHRF was upregulated in myocardial I/R injury models. Suppression of CHRF relieved myocardial I/R injury in vivo. In addition, in vitro silencing of CHRF enhanced cell viability and attenuated lactate dehydrogenase activity (LDH) as well as apoptosis in H9C2 cells treated with hypoxia/reoxygenation injury. Autophagy has been studied to play an important role in myocardial I/R injury. Thus, experiments related to autophagy were done, and the results showed that CHRF knockdown decreased autophagy. For the exploration of the regulatory mechanism, we found that CHRF sequestered and negatively regulated miR‐182‐5p to release its inhibition on ATG7. Findings from rescue assays revealed that ATG7 overexpression could suppress the effects of CHRF silence on cell viability, LDH level, apoptosis, and autophagy. To sum up, our results suggested that CHRF exacerbated myocardial I/R injury by enhancing autophagy via modulation of the miR‐182‐5p/ATG7 pathway. Therefore, this competing endogenous RNA axis may be a potential therapeutic biomarker for myocardial I/R injury.

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Long non‑coding RNA, CHRF, predicts poor prognosis of lung adenocarcinoma and promotes cell proliferation and migration

Cited by 3 publications

References 31 publications

Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases

Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases

LncRNAs Affecting NF-κB-Mediated Macrophage Inflammation Are Potential Therapeutic Targets in Human Diseases

LncRNA CHRF aggravates myocardial ischemia/reperfusion injury by enhancing autophagy via modulation of the miR‐182‐5p/ATG7 pathway

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