Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma

Shen, Ying; Feng, Yuandong; Chen, Hongli; Huang, Lingjuan; Wang, Fangxia; Bai, Jing; Yang, Yun; Wang, Jianli; Zhao, Wanhong; Yin, Jianfei; Peng, Ying; Lei, Xiaoru; He, Aili

doi:10.1016/j.lfs.2018.01.025

Cited by 22 publications

(31 citation statements)

References 28 publications

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“…A cohort of 34 patients who were diagnosed with myeloma at their first clinical visits and admitted to the Affiliated Hospital of Nantong University (Nantong, China) between February 2015 and July 2018 were included in this study. The diagnosis, stage and risk status of MM were made in accordance with the National Comprehensive Cancer Network (NCCN) (2015 version 3 and 2017 version 3) . All patients in this research were newly diagnosed without being administered with any treatment.…”

Section: Methodsmentioning

confidence: 99%

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PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

Shen

Kong

Yang

et al. 2020

J Cellular Molecular Medi

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Loss of one or some specific miRNA‐mediated regulation is closely associated with malignant progression of multiple myeloma (MM). But how these miRNAs work and what role the specific miRNA plays in this process of malignant progression remain unclear. It was found in this study that the expression of miR‐129 was decreased in both MM cell lines and newly diagnosed MM patients. Further clinicopathological statistics showed that miR‐129 was correlated with the isotype of MM patients. MiR‐129 overexpression disturbed cell proliferation, cell cycle evolution and spurred apoptosis both in vitro and in vivo. MAP3K7, a kinase able to activate NF‐κB circuit, was found to be up‐regulated in MM and contain a binding target of miR‐129. In addition, lncRNA PCAT‐1 functioned to sponge miR‐129 and thereby lowered its expression. PCAT‐1 knockdown eliminated the tumour‐promoting effect caused by miR‐129 inhibition, probably through repressing MAP3K7 and subsequent NF‐κB activation. To the best of our knowledge, this is the first study to have discovered that increased expression of PCAT‐1 could augment cell proliferation and cycle procession and inhibit apoptosis by down‐regulating miR‐129 via the MAP3K7/NF‐κB pathway in MM.

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Section: Methodsmentioning

confidence: 99%

“…The diagnosis, stage and risk status of MM were made in accordance with the National Comprehensive Cancer Network (NCCN) (2015 version 3 and 2017 version 3). 11 All patients in this research were newly diagnosed without being administered with any treatment. Mononuclear…”

Section: Patientsmentioning

confidence: 99%

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

Shen

Kong

Yang

et al. 2020

J Cellular Molecular Medi

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“…One of the SNPs identified in our study (rs9858592) is in strong LD (r 2 > 0.8) with two intronic ST3GAL6AS1 SNPs (rs4857414 and rs12635955) previously reported on the NCBI database to be associated with circulating sgp130 (https://www.ncbi.nlm.nih.gov/projects/ SNP/GaPBrowser_prod/callGaPBrowser2.cgi?snp= 828588&aid=3748). ST3GAL6AS1 codes for a long noncoding RNA, possibly involved in the regulation of the expression of a sialyltransferase, ST3GAL6 [28]. Sialylation contributes to regulation of cell adhesion and is recognized as one of the cellular mechanisms promoting atherosclerosis [29].…”

Section: Discussionmentioning

confidence: 99%

Analysis of the genetic variants associated with circulating levels of sgp130. Results from the IMPROVE study

et al. 2020

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The genes regulating circulating levels of soluble gp130 (sgp130), the antagonist of the inflammatory response in atherosclerosis driven by interleukin 6, are largely unknown. Aims of the present study were to identify genetic loci associated with circulating sgp130 and to explore the potential association between variants associated with sgp130 and markers of subclinical atherosclerosis. The study is based on IMPROVE (n = 3703), a cardiovascular multicentre study designed to investigate the determinants of carotid intima media thickness, a measure of subclinical atherosclerosis. Genomic DNA was genotyped by the CardioMetaboChip and ImmunoChip. About 360,842 SNPs were tested for association with log-transformed sgp130, using linear regression adjusted for age, gender, and population stratification using PLINK v1.07. A p value of 1 × 10 −5 was chosen as threshold for significance value. In an exploratory analysis, SNPs associated with sgp130 were tested for association with c-IMT measures. We identified two SNPs significantly associated with sgp130 levels and 24 showing suggestive association with sgp130 levels. One SNP (rs17688225) on chromosome 14 was positively associated with sgp130 serum levels (β = 0.03 SE = 0.007, p = 4.77 × 10 −5 ) and inversely associated with c-IMT (c-IMT mean-max β = −0.001 SE = 0.005, p = 0.0342). Our data indicate that multiple loci regulate sgp130 levels and suggest a possible common pathway between sgp130 and c-IMT measures.

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“…Our previous study identified MM-associated lncRNAs using gene chip technology and bioinformatics databases. The results showed that 2,445 lncRNAs were upregulated, and 1,519 lncRNAs were downregulated, in five newly diagnosed MM bone marrow samples compared to iron deficiency anemia (IDA) controls by Arraystar Human LncRNA Array v.4.0 gene chip analysis [9]. However, we only reported four differentially expressed lncRNAs in that article.…”

Section: Introductionmentioning

confidence: 99%

High Expression Levels of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 and Semaphorin 5A Indicate Poor Prognosis in Multiple Myeloma

et al. 2019

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Background: The aim of this study was to detect the expression of long noncoding RNA small nucleolar RNA host gene 18 (SNHG18) andsemaphorin 5A (SEMA5A) genes in multiple myeloma (MM) patients and to explore the correlation of the expression of these genes with the clinical characteristics and prognosis of MM patients. Methods: Forty-seven newly diagnosed MM, 18 complete remission MM, 13 refractory/relapse MM, and 22 iron deficiency anemia (serving as control) samples were extracted at the Department of Hematology, Second Aﬃliated Hospital of Xian Jiaotong University between January 2015 and December 2016. The clinical features of the MM patients are summarized. Real-time quantitative PCR was performed to analyze the relative expression levels of the SNHG18 and SEMA5Agenes. The clinical characteristics and overall survival (OS) of the MM patients were statistically analyzed while measuring different levels of SNHG18 and SEMA5Agene expression. At the same time, the correlation between the expression of SNHG18 and SEMA5A was also analyzed. Results: The analysis confirmed that SNHG18 and its possible target gene SEMA5A were both highly expressed in newly diagnosed MM patients. After analyzing the clinical signiﬁcance of SNHG18 and SEMA5A in MM patients, we found that the expression of SNHG18 and SEMA5A was related to the Durie-Salmon (DS), International Staging System (ISS), and Revised International Staging System (R-ISS) classification systems, and the Mayo Clinic Risk Stratification for Multiple Myeloma (mSMART; p < 0.05). Moreover, we observed a significant difference in OS between the SNHG18/SEMA5A high expression group and the low expression group. We found a positive correlation between SNHG18 and SEMA5A expression (r = 0.709, p < 0.01). Surprisingly, the expected median OS times of both the SNHG18 and SEMA5Ahigh expression groups were significantly decreased, which was in contrast to those of both the SNHG18 and SEMA5Alow expression groups and the single-gene high expression group (p < 0.05). Conclusion: High expression of both SNHG18 and SEMA5A is associated with poor prognosis in patients with MM.

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Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma

Abstract: These results reveal the feasible functions of lncRNAs in pathogenesis of MM. Further studies are required to explore whether these lncRNAs could serve as candidate therapeutic targets and new molecular biomarkers for MM.

Cited by 22 publications

References 28 publications

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

Analysis of the genetic variants associated with circulating levels of sgp130. Results from the IMPROVE study

High Expression Levels of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 and Semaphorin 5A Indicate Poor Prognosis in Multiple Myeloma

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