hTERT mediates gastric cancer metastasis partially through the indirect targeting of ITGB1 by microRNA-29a

He, Bing; Xiao, Yufeng; Tang, Bo; Wu, Yingyi; Hu, C.; Xie, Rui; Yang, Xinquan; Yu, Songtao; Dong, Hui; Zhao, Xiao‐Fan; Li, Jiliang; Yang, Shiming

doi:10.1038/srep21955

Cited by 49 publications

(50 citation statements)

References 33 publications

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“…PXDN levels were found to be elevated in primary glial and secondary metastatic brain tumours as well as in its immediate microvasculature (Liu et al ., 2010). Similarly, ITGB1, a cell adhesive molecule, which functions to mediate association between cells and the ECM, has also been found to be misregulated in various cancers and found to impact malignant phenotypes such as invasion, proliferation and angiogenesis (He et al ., 2016; Zhang and Zou, 2015). A study also suggested the role of ITGB1 in the secretion and activation of MMP14 (Mori et al ., 2013).…”

Section: Discussionmentioning

confidence: 99%

Impact of somatic copy number alterations on the glioblastoma miRNome: miR‐4484 is a genomically deleted tumour suppressor

et al. 2017

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Glioblastoma (GBM) is the most frequent and most malignant primary brain tumour in adults. GBMs have a unique landscape of somatic copy number alterations (SCNAs), with the concomitant appearance of numerous driver amplifications and deletions. Here, we examined the genomic regions harbouring SCNAs and their impact on the GBM miRNome. We found that 40% of SCNA events covering 70–88% of the genomically altered regions, as identified by GISTIC and RAE algorithms, carried miRNA genes. Of 1426 annotated mature miRNAs analysed, ~ 14% (n = 198) were mapped to such fragile loci. Further, we identified an intragenic miRNA, miR‐4484 located on chromosome‐10, as a deleted and downregulated miRNA in GBM. miR‐4484 exhibited a strong positive correlation with the expression of its host gene uroporphyrinogen III synthase (UROS), thereby indicating that the loss of miR‐4484 is a codeletion event in GBM. Overexpression of miR‐4484 reduced the colony‐forming ability and suppressed the migratory capacity of glioma cells. Analysis of the RNA‐seq‐derived transcriptome upon exogenous miR‐4484 overexpression in conjunction with an integrative bioinformatics approach revealed several putative targets of miR‐4484. Unbiased functional enrichment of these targets through DAVID identified a cohort of important gene ontology terms, which possibly explain the functional role of miR‐4484 in gliomagenesis. Selected targets were validated and, importantly, were found to be upregulated in GBM. In brief, our study identified a panel of miRNAs that are likely to be regulated by genomic deletions and amplifications. Further, miR‐4484 was found to be deleted and acts as a tumour suppressor miRNA in GBM.

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Section: Discussionmentioning

confidence: 99%

Impact of somatic copy number alterations on the glioblastoma miRNome: miR‐4484 is a genomically deleted tumour suppressor

et al. 2017

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“…Integrin β1 (ITGB1) is a type of cell adhesion molecule that mediates mutual adhesion between cells and Extracellular Matrix (ECM). ITGB1 is often abnormally expressed in tumors and is implicated in aberrant proliferation, angiogenesis, invasion and metastasis [33–34]. Hypoxia-inducible factor 1a (HIF1a) is an essential transcription factor for cellular adaptation to hypoxia in cancer [35–36].…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Long Noncoding RNA and mRNA Expression Profile in Advanced Laryngeal Squamous Cell Carcinoma

Wang

Lian

et al. 2016

PLoS ONE

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Long non-coding RNA (lncRNA) plays an important role in tumorigenesis. However, the expression pattern and function of lncRNAs in laryngeal squamous cell carcinoma (LSCC) are still unclear. To investigate the aberrantly expressed lncRNAs and mRNAs in advanced LSCC, we screened lncRNA and mRNA expression profiles in 9 pairs of primary Stage IVA LSCC tissues and adjacent non-neoplastic tissues by lncRNA and mRNA integrated microarrays. Gene Ontology and pathway analysis were performed to find out the significant function and pathway of the differentially expressed mRNAs, gene-gene functional interaction network and ceRNA network were constructed to select core mRNAs, and lncRNA-mRNA expression correlation network was built to identify the interactions between lncRNA and mRNA. qRT-PCR was performed to further validate the expressions of selected lncRNAs and mRNAs in advanced LSCC. We found 1459 differentially expressed lncRNAs and 2381 differentially expressed mRNAs, including 846 up-regulated lncRNAs and 613 down-regulated lncRNAs, 1542 up-regulated mRNAs and 839 down-regulated mRNAs. The mRNAs ITGB1, HIF1A, and DDIT4 were selected as core mRNAs, which are mainly involved in biological processes, such as matrix organization, cell cycle, adhesion, and metabolic pathway. LncRNA-mRNA expression correlation network showed LncRNA NR_027340, MIR31HG were positively correlated with ITGB1, HIF1A respectively. LncRNA SOX2-OT was negatively correlated with DDIT4. qRT-PCR further validated the expression of these lncRNAs and mRNAs. The work provides convincing evidence that the identified lncRNAs and mRNAs are potential biomarkers in advanced LSCC for further future studies.

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“…To date, there are numerous studies establishing the role of hTERT in invasion and metastasis in several tumor types such as urological tumors [14][15][16][17][18], melanomas [16,19,20], gastric cancer [21][22][23][24], gliomas [15,[25][26][27][28], and hepatocellular tumors, but only very few investigated the mechanism behind this observed pattern or this coherence.…”

Section: Role Of Telomerase Reverse Transcriptase In Cancer Metastasismentioning

confidence: 99%

Essential roles of telomerase reverse transcriptase hTERT in cancer stemness and metastasis

Hannen

Bartsch

2018

FEBS Letters

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Maintenance of chromosomal telomere length is a hallmark of cancer cells and a prerequisite for stemness. In 85-90% of all human cancers, telomere length maintenance is achieved by reactivation of telomerase, whereas in the remaining 10-15% cancers, alternative lengthening of telomeres (ALT) is observed. Reactivation of telomerase occurs by various mechanisms, one of which is accumulation of point mutations in the promoter region of the gene encoding the protein subunit hTERT. There are numerous studies linking either hTERT overexpression or the presence of hTERT mutations to an aggressive phenotype of several human cancers. Recent findings demonstrate that hTERT expression is not only associated with replicative immortality, but also with cancer cell motility and stem cell phenotype. However, the mechanisms by which hTERT affects cancer cell migration, invasion, and distant metastasis on the one hand, and stemness and resistance on the other hand, are still poorly understood. Within this review, we aim to provide an overview on the functional involvement of hTERT in these cellular processes, focusing on metastasis formation and maintenance of stemness in different human cancers.

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hTERT mediates gastric cancer metastasis partially through the indirect targeting of ITGB1 by microRNA-29a

Cited by 49 publications

References 33 publications

Impact of somatic copy number alterations on the glioblastoma miRNome: miR‐4484 is a genomically deleted tumour suppressor

Impact of somatic copy number alterations on the glioblastoma miRNome: miR‐4484 is a genomically deleted tumour suppressor

Integrated Analysis of Long Noncoding RNA and mRNA Expression Profile in Advanced Laryngeal Squamous Cell Carcinoma

Essential roles of telomerase reverse transcriptase hTERT in cancer stemness and metastasis

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