Long Noncoding RNA AFAP1-AS1 Promotes Cell Proliferation and Metastasis via the miR-155-5p/FGF7 Axis and Predicts Poor Prognosis in Gastric Cancer

Ma, Hong-Wu; Xi, Dayong; Ma, Jianzhong; Guo, Min; Ma, Li; Ma, Dong-Hong; Li, Peiwu; Guo, Changan

doi:10.1155/2020/8140989

Cited by 22 publications

(18 citation statements)

References 32 publications

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“…Zhu et al reported that FGF7 could promote breast cancer progression through AKT signaling pathway [ 39 ]. In GC, several studies indicated that FGF7 might play a role in GC cell proliferation and metastasis [ 40 , 41 ]. The product of gene NPR3 encodes one of the natriuretic peptide receptors and responsible of clearing natriuretic peptides.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of tumor mutation burden and immune microenvironment in gastric cancer

Zhang

Wang

et al. 2021

Bioscience Reports

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Tumor mutation burden (TMB) was a promising marker for immunotherapy. We aimed to investigate the prognostic role of TMB and its relationship with immune cells infiltration in gastric cancer (GC). We analyzed the mutation landscape of all GC cases and TMB of each GC patient was calculated and patients were divided into TMB-high and TMB-low group. Differentially expressed genes (DEGs) between the two groups were identified and pathway analysis was performed. The immune cells infiltration in each GC patient was evaluated and Kaplan-Meier analysis was performed to investigate the prognostic role of immune cells infiltration. At last, hub immune genes were identified and a TMB prognostic risk score (TMBPRS) was constructed to predict the survival outcome of GC patients. The relationships between mutants of hub immune genes and immune infiltration level in GC was investigated. We found higher TMB was correlated with better survival outcome and female patients, patients with T1-2 and N0 had higher TMB score. Altogether 816 differentially expressed genes were harvested and pathway analysis demonstrated that patients in TMB-high group were associated with neuroactive ligand-receptor interaction, cAMP signaling pathway, calcium signaling pathway. The infiltration of activated CD4+ memory T cells, follicular helper T cells, resting NK cells, M0 and M1 macrophages and neutrophils in TMB-high group were higher compared than that in TMB-low group and high macrophage infiltration was correlated with inferior survival outcome of GC patients. Last, the TMBPRS was constructed and GC patients with high TMBPRS had poor prognosis.

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Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of tumor mutation burden and immune microenvironment in gastric cancer

Zhang

Wang

et al. 2021

Bioscience Reports

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“…It is the subcellular localization of NATs that are closely related to their different mechanisms of biological functions ( Bergalet et al, 2020 ). Normally, nuclear NATs are mainly involved in transcriptional interference, epigenetic modifications, RNA pocessing and alternative splicing, whereas cytoplasmic NATs are mainly involved in RNA stability and/or mRNA translatability ( Xu et al, 2019 ; Ma et al, 2020 ; Xu et al, 2020 ). Therefore we examined the subcellular localization and the protein coding potential of Nqo1-AS1.…”

Section: Discussionmentioning

confidence: 99%

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

et al. 2021

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Evidence of the involvement of long noncoding RNAs (lncRNAs) in the pathogenesis of chronic obstructive pulmonary disease (COPD) is growing but still largely unknown. This study aims to explore the expression, functions and molecular mechanisms of Fantom3_F830212L20, a lncRNA that transcribes in an antisense orientation to Nqo1.We name this lncRNA as Nqo1 antisense transcript 1 (Nqo1-AS1). The distribution, expression level and protein coding potential of Nqo1-AS1 were determined. The effects of Nqo1-AS1 on cigarette smoke (CS)-induced oxidative stress were also evaluated. The results showed that Nqo1-AS1 were mainly located in the cytoplasm of mouse alveolar epithelium and had a very low protein coding potential. Nqo1-AS1 (or its human homologue) was increased with the increase of CS exposure. Nqo1-AS1 overexpression enhanced the mRNA and protein levels of Nqo1 and Serpina1 mRNA expression, and attenuated CS-induced oxidative stress, whereas knockdown of Nqo1-AS1 significantly decreased Nqo1 and Serpina1 mRNA expressions, and aggravated CS-induced oxidative stress. Nqo1-AS1 increased Nqo1 mRNA stability and upregulated Nqo1 expression through antisense pairing with Nqo1 3′UTR. In conclusion, these results suggest that Nqo1-AS1 attenuates CS-induced oxidative stress by increasing Nqo1 mRNA stability and upregulating Nqo1 expression, which might serve as a novel approach for the treatment of COPD.

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“… 35 , 36 In addition, work in GC cells has indicated that lncRNA AFAP1-AS1 promotes proliferation and metastasis via miR-155-5p/FGF7 regulatory axis. 37 In this study, Linc-ROR was negatively correlated with miR-212-3p, while Linc-ROR was positively correlated with FGF7 expression in gastric tissues. Further, the dual-luciferase reporter assay confirmed that the direct interaction between Linc-ROR and miR-212-3p, miR-212-3p and FGF7 3ʹUTR mRNA.…”

Section: Discussionmentioning

confidence: 46%

Upregulation of Linc-ROR Promotes the Proliferation, Migration, and Invasion of Gastric Cancer Cells Through miR-212-3p/FGF7 Axis

Mi¹,

Li²,

He³

et al. 2021

CMAR

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Background Linc-ROR is a long non-coding RNA, that is found aberrantly expressed in various human cancers. We aim here to unveil the role of Linc-ROR in gastric cancer (GC) progression. Methods qPCR was used to determine gene expression. Cell viability was measured by CCK-8 assay. Transwell assays were performed to evaluate the GC cells’ migratory and invasive abilities. Xenograft mouse model was conducted to measure tumor growth. Results We found that Linc-ROR were overexpressed in GC tissues compared to the adjacent tissues. High Linc-ROR predicts poor prognosis of GC patients. The prediction of bioinformatics online revealed that Linc-ROR could bind to miR-212-3p. Further, dual-luciferase reporter assay confirmed a direct interaction between Linc-ROR and miR-212-3p. Overexpression of miR-212-3p facilitated GC cells’ migration and invasion, while the silencing of miR-212-3p attenuated GC cell migratory and invasive abilities. Moreover, Linc-ROR knockdown significantly suppressed the proliferation, migration, and invasion of GC cells, whereas miR-212-3p antagomir partially reversed Linc-ROR knockdown-induced phenotypes. Fibroblast growth factor 7 (FGF7), a downstream molecule of miR-212-3p, was overexpressed in GC cells. The recovery of FGF7 expression partially reversed the phenotypes caused by Linc-ROR silencing. Mechanistically, silencing of Linc-ROR contributed to the downregulation of CDK4, CDK6, Cyclin D1, N-Cadherin, Vimentin, MMP-9, MMP-2, but caused the upregulation of P21, P27, E-Cadherin, CK-19 in MGC-803 cells; however, FGF7 treatment could reverse the results induced by Linc-ROR silencing. Results in vivo further suggested that Linc-ROR knockdown repressed GC tumor growth, where the expression of miR-212-3p was up-regulated and FGF7 expression was downregulated in tumor tissues of mice. Conclusion These findings indicated that Linc-ROR/miR-212-3p/FGF7 axis played an important role in gastric cancer progression. Linc-ROR expression level was associated with the prognosis of GC patients.

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Long Noncoding RNA AFAP1-AS1 Promotes Cell Proliferation and Metastasis via the miR-155-5p/FGF7 Axis and Predicts Poor Prognosis in Gastric Cancer

Cited by 22 publications

References 32 publications

Comprehensive analysis of tumor mutation burden and immune microenvironment in gastric cancer

Comprehensive analysis of tumor mutation burden and immune microenvironment in gastric cancer

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

Upregulation of Linc-ROR Promotes the Proliferation, Migration, and Invasion of Gastric Cancer Cells Through miR-212-3p/FGF7 Axis

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