Diagnostic value of strand‐specific mi<scp>RNA</scp>‐101‐3p and mi<scp>RNA</scp>‐101‐5p for hepatocellular carcinoma and a bioinformatic analysis of their possible mechanism of action

Yang, Xia; Pang, Yu‐Yan; He, Rong‐Quan; Lin, Peng; Cen, Jiemei; Yang, Hong; Ma, Jie; Chen, Gang

doi:10.1002/2211-5463.12349

Cited by 22 publications

(12 citation statements)

References 67 publications

(66 reference statements)

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“…Among two mature miRNAs, miR-101-3p is generated from the 3′-ends of the precursor, and miR-101-5p is generated from the 5′-end of pre-miR-101 34. Accumulating evidence have demonstrated that the levels of miR-101-5p are decreased in many malignances, including liver cancer 35. In NSCLC, miR-101-3p suppresses the growth and metastasis of cancer cells via blocking the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and regulating the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) 14.…”

Section: Discussionmentioning

confidence: 99%

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Chen¹,

Liú²,

Zhang³

et al. 2019

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BackgroundThe purpose of this study is to explore the potential biological roles of miR-101-5p in the progression of non-small-cell lung carcinoma (NSCLC).MethodsThe levels of miR-101-5p and chemokine (C-X-C motif) ligand 6 (CXCL6) in NSCLC tissues and cells were detected using the quantitative real-time PCR (qRT-PCR) assay. Proliferation, colony formation, migration and invasion assays were conducted using miR-101-5p-transfected NSCLC cells in vitro. The expression of CXCL6 was measured using immunofluorescence assay. Xenograft model and lung metastasis model were constructed to further reveal the precise roles of miR-101-5p in the lung metastasis and growth of NSCLC cells in vivo.ResultsmiR-101-5p was underregulated in NSCLC tissues when compared with that in the normal controls. The levels of miR-101-5p were lower in NSCLC cells (H1975, A549, HCC827 and H1650) than in non-tumorigenic human bronchial epithelial cells (BEAS-2B). Overregulation of miR-101-5p restrained the aggressiveness phenotypes of NSCLC cells in vitro. Furthermore, overregulation of miR-101-5p reduced the tumor growth and pulmonary metastasis of NSCLC cells in vivo. CXCL6 was the target gene of miR-101-5p in NSCLC. The mRNA levels of CXCL6 were negatively associated with the levels of miR-101-5p in NSCLC tissues. Finally, the rescue experiments suggested that the inhibitory role of miR-101-5p was mediated by regulating the expression of CXCL6 in NSCLC.ConclusionThese findings indicated that overregulation of miR-101-5p restrained the progression of NSCLC cells by targeting CXCL6 and might function as a potential therapeutic target for NSCLC.

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Section: Discussionmentioning

confidence: 99%

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Chen¹,

Liú²,

Zhang³

et al. 2019

OTT

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“…MicroRNAs (miRNAs) are small, non-coding RNA molecules of ~ 22 nucleotides, which perform functions in the post-transcriptional regulation of gene expression ( 11 – 15 ). miRNAs act as oncogenes or antioncogenes in tumorigenesis, thus influencing the onset and development of tumors ( 16 – 20 ). Previous studies have shown that the downregulated expression of miRNA may be essential in the onset and development of PCa ( 21 – 23 ).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR‑224‑5p in prostate cancer and its relevant molecular mechanism via TCGA, GEO database and in�silico analyses

Gan

Zhang

et al. 2018

Oncol Rep

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The function of the expression of microRNA (miR)-224-5p in prostate adenocarcinoma (PCa) remains to be elucidated, therefore, the present study aimed to investigate the clinical significance and potential molecular mechanism of miR-224-5p in PCa. Data on the expression of miR-224-5p in PCa were extracted from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), ArrayExpress and previous literature, and meta-analyses with standardized mean difference (SMD) and summary receiver operating characteristic (sROC) methods were performed for statistical analyses. The prospective target genes of miR-224-5p were collected by overlapping the differentially expressed mRNAs in TCGA and GEO, and target genes predicted by miRWalk2.0. Subsequently, in silico analysis was performed to examine the associated pathways of miR-224-5p in PCa. The expression of miR-224-5p was markedly lower in PCa; the overall SMD was −0.562, and overall sROC area under the curve was 0.80. In addition, Kyoto Encyclopedia of Genes and Genomes analysis revealed that the prospective target genes of miR-224-5p were largely enriched in the amino sugar and nucleotide sugar metabolism signaling pathway, and three genes [UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1), hexokinase 2 (HK2) and chitinase 1 (CHIT1)] enriched in this pathway showed higher expression (P<0.05). In addition, key genes in the protein-protein interaction network analysis [DNA topoisomerase 2-α (TOP2A), ATP citrate lyase (ACLY) and ribonucleotide reductase regulatory subunit M2 (RRM2)] exhibited significantly increased expression (P<0.05). The results suggested that the downregulated expression of miR-224-5p may be associated with the clinical progression and prognosis of PCa. Furthermore, miR-224-5p likely exerts its effects by targeting genes, including UAP1, HK2, CHIT1, TOP2A, ACLY and RRM2. However, in vivo and in vitro experiments are required to confirm these findings.

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“…Where SE represents sensitivity; SP represents specificity; TP+FN is the sample size of the tumour; and FP+TN is the sample size of the normal control. The meta-analysis was performed using STATA 12.0 (StataCorp LP, College Station, TX, USA) for pooling the standardized mean difference (SMD), sensitivity, specificity and summary ROC of HOXA11 expression ( 16 , 17 ). An I 2 test was used to evaluate heterogeneity, when I 2 <50%, a fixed-effects model was used; while I 2 ≥50% the random-effects model was selected ( 18 ).…”

Section: Methodsmentioning

confidence: 99%

Upregulation of HOXA11 during the progression of lung adenocarcinoma detected via multiple approaches

Yang

Deng

et al. 2018

Int J Mol Med

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The altered expression of homeobox (HOX)A11 has been observed in various malignant tumor types, but it has remained to be determined in human lung adenocarcinoma (LUAD). In the present study, the expression of HOXA11 in LUAD and the potential associated mechanisms were assessed. Data from The Cancer Genome Atlas and Oncomine microarrays were gathered and in-house polymerase chain reaction data were produced to investigate the altered expression of HOXA11 in LUAD and its association with various clinicopathological characteristics. Genes co-expressed with HOXA11 were also identified by searching the cBioPortal and Multi Experiment Matrix databases, and performing a bioinformatics analysis, through which the potential molecular mechanisms of HOXA11 in LUAD were explored. The data analyses indicated that HOXA11 was overexpressed in the LUAD samples, and together with its co-expressed genes, it was indicated to participate in various key signaling pathways, including the focal adhesion, extracellular matrix-receptor interaction, axon guidance and small cell lung cancer signaling pathways. Furthermore, collagen type III α 1 chain (COL3A1), ephrin B2 (EFNB2), integrin subunit α 8 (ITGA8) and syndecan 2 (SDC2) were confirmed to be differentially expressed in LUAD vs. normal controls at the mRNA and protein level. Of note, LUAD patients with low expression of HOXA11 and ITGB1 had better overall survival rates. The present study indicated that HOXA11 may function as an oncogene in LUAD, and HOXA11 protein probably combines with ITGB1, COL3A1, EFNB2, ITGA8 and SDC2 to have a role in the focal adhesion pathway.

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Diagnostic value of strand‐specific miRNA‐101‐3p and miRNA‐101‐5p for hepatocellular carcinoma and a bioinformatic analysis of their possible mechanism of action

Cited by 22 publications

References 67 publications

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Downregulation of miR‑224‑5p in prostate cancer and its relevant molecular mechanism via TCGA, GEO database and in�silico analyses

Upregulation of HOXA11 during the progression of lung adenocarcinoma detected via multiple approaches

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