Downregulation of lncRNA FGF12-AS2 suppresses the tumorigenesis of NSCLC via sponging miR-188-3p

Zhou, Lili; Chen, Xing; Zhou, Dansha; Yang, Rui; Cai, Maohuai

doi:10.1515/med-2020-0219

Cited by 8 publications

(4 citation statements)

References 42 publications

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“…In the previous studies, NPSR1 ‐ AS1 had been reported as the poor prognosis markers for LUAD 26 ; SATB2 ‐ AS1 could be broadly involved in multiple cancer development 27 , 28 , 29 ; FGF12 ‐ AS2 may be served as a potential target for the treatment of non‐small‐cell lung carcinoma. 30 The evidence further highlighted the PR‐lncRNA signature might exert an essential contribution for LUAD processes and have the potential clinical utility.…”

Section: Resultsmentioning

confidence: 93%

Immune‐related eight‐lncRNA signature for improving prognosis prediction of lung adenocarcinoma

Chen

Zhang

et al. 2021

Clinical Laboratory Analysis

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Background Lung adenocarcinoma (LUAD) is the leading cause of cancer‐related deaths worldwide. Therefore, the identification of a novel prediction signature for predicting the prognosis risk and survival outcomes is urgently demanded. Methods We integrated a machine‐learning frame by combing the Cox regression and Least Absolute Shrinkage and Selection Operator (LASSO) regression model to identify the LUAD‐related long non‐coding RNA (lncRNA) survival biomarkers. Subsequently, the Spearman correlation test was employed to interrogate the relationships between lncRNA signature and tumor immunity and constructed the competing endogenous RNA (ceRNA) network. Results Herein, we identified an eight‐lncRNA signature (PR‐lncRNA signature, NPSR1‐AS1, SATB2‐AS1, LINC01090, FGF12‐AS2, AC005256.1, MAFA‐AS1, BFSP2‐AS1, and CPC5‐AS1), which contributes to predicting LUAD patient's prognosis risk and survival outcomes. The PR‐lncRNA signature has also been confirmed as the robust signature in independent datasets. Further parsing of the LUAD tumor immune infiltration showed the PR‐lncRNAs were closely associated with the abundance of multiple immune cells infiltration and the expression of MHC molecules. Furthermore, by constructing the PR‐lncRNA–related ceRNA network, we interrogated more potential anti‐cancer therapy targets. Conclusion lncRNAs, as emerging cancer biomarkers, play an important role in a variety of cancer processes. Identification of PR‐lncRNA signatures allows us to better predict patient's survival outcomes and disease risk. Finally, the PR‐lncRNA signatures could help us to develop novel LUAD anti‐cancer therapeutic strategies.

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Section: Resultsmentioning

confidence: 93%

Immune‐related eight‐lncRNA signature for improving prognosis prediction of lung adenocarcinoma

Chen

Zhang

et al. 2021

Clinical Laboratory Analysis

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“…Besides, lncRNA insulin growth factor 2 antisense(IGF2AS) is not only an imprinted gene in Wilms tumors involved in the transcription and translation of a variety of proteins but also a low-expressing lncRNA in NSCLC tissues, which is closely related to the overall survival of patients and a potent inhibitor to the migration of NSCLC cells [39]. Unlike mouse IGF-2AS, human IGF-2AS likely encodes a putative peptide consisting of 273 amino acids [40,41]. IGF-2AS transcripts are mainly present in the cytoplasm and are associated with polysomes, suggesting that the mechanism by which IGF-2AS is involved in tumor progression may be related to the regulation of protein translation [40,41].…”

Section: Lncrna Related To Nsclc Treatmentmentioning

confidence: 99%

“…Unlike mouse IGF-2AS, human IGF-2AS likely encodes a putative peptide consisting of 273 amino acids [40,41]. IGF-2AS transcripts are mainly present in the cytoplasm and are associated with polysomes, suggesting that the mechanism by which IGF-2AS is involved in tumor progression may be related to the regulation of protein translation [40,41].…”

Section: Lncrna Related To Nsclc Treatmentmentioning

confidence: 99%

LncRNA in tumorigenesis of non-small-cell lung cancer: From bench to bedside

Chen

et al. 2022

Cell Death Discov.

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Lung cancer has been one of the leading causes of cancer-related death worldwide, and non-small-cell lung cancer (NSCLC) accounts for the majority of lung cancer morbidity, yet the pathogenesis of NSCLC has not been fully elucidated. Recently, long-chain non-coding RNA (lncRNA) has attracted widespread attention. LncRNA is a type of non-coding RNA whose transcript length exceeds 200 nucleotides. After constant research, academics updated their understanding of lncRNA, especially its role in the biological processes of cancer cells, including epigenetic regulation, cell proliferation, and cell differentiation. Notably, examination of lncRNAs could serve as potential hallmarks for clinicopathological features, long-term prognosis, and drug sensitivity. Therefore, it is necessary to explore the functions of lncRNA in NSCLC and innovate potential strategies against NSCLC based on lncRNA-related research. Herein, we reviewed the functions of lncRNA in the occurrence, diagnosis, treatment, and prognosis of NSCLC, which not only help promote a comprehensive view of lncRNA in NSCLC, but also shed light on the potential of lncRNA-based diagnosis and treatment of NSCLC.

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“…Several of these studies have also reported altered miR-188-3p expression in various human cancers, including gastric cancer[ 12 - 22 ]. For example, miR-183-3p expression was reduced in non-small cell lung cancer vs. normal tissues, whereas miR-188-3p overexpression inhibited tumor cell proliferation and colony formation[ 14 , 16 ]. MiR-183-3p expression was also reduced in human hepatocellular carcinoma compared to normal tissues.…”

Section: Introductionmentioning

confidence: 99%

Antitumor activity of miR-188-3p in gastric cancer is achieved by targeting CBL expression and inactivating the AKT/mTOR signaling

Lin¹,

Luo²,

Su³

et al. 2023

World J Gastrointest Oncol

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Colitis-associated colorectal cancer (CAC) is defined as a specific cluster of colorectal cancers that develop as a result of prolonged colitis in patients with inflammatory bowel disease (IBD). Patients with IBD, including ulcerative colitis and Crohn’s disease, are known to have an increased risk of developing CAC. Although the incidence of CAC has significantly decreased over the past few decades, individuals with CAC have increased mortality compared to individuals with sporadic colorectal cancer, and the incidence of CAC increases with duration. Chronic inflammation is generally recognized as a major contributor to the pathogenesis of CAC. CAC has been shown to progress from colitis to dysplasia and finally to carcinoma. Accumulating evidence suggests that multiple immune-mediated pathways, DNA damage pathways, and pathogens are involved in the pathogenesis of CAC. Over the past decade, there has been an increasing effort to develop clinical approaches that could help improve outcomes for CAC patients. Colonoscopic surveillance plays an important role in reducing the risk of advanced and interval cancers. It is generally recommended that CAC patients undergo endoscopic removal or colectomy. This review summarizes the current understanding of CAC, particularly its epidemiology, mechanisms, and management. It focuses on the mechanisms that contribute to the development of CAC, covering advances in genomics, immunology, and the microbiome; presents evidence for management strategies, including endoscopy and colectomy; and discusses new strategies to interfere with the process and development of CAC. These scientific findings will pave the way for the management of CAC in the near future.

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Downregulation of lncRNA FGF12-AS2 suppresses the tumorigenesis of NSCLC via sponging miR-188-3p

Cited by 8 publications

References 42 publications

Immune‐related eight‐lncRNA signature for improving prognosis prediction of lung adenocarcinoma

Immune‐related eight‐lncRNA signature for improving prognosis prediction of lung adenocarcinoma

LncRNA in tumorigenesis of non-small-cell lung cancer: From bench to bedside

Antitumor activity of miR-188-3p in gastric cancer is achieved by targeting CBL expression and inactivating the AKT/mTOR signaling

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