Families of microRNAs Expressed in Clusters Regulate Cell Signaling in Cervical Cancer

Servín-González, Luis Steven; Granados-López, Angélica Judith; López, Jesús Adrián

doi:10.3390/ijms160612773

Cited by 42 publications

(45 citation statements)

References 73 publications

(95 reference statements)

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“…In present study, we found that miR-106a was significantly upregulated in CC tissue samples and cell lines, which was consistent with previous microarray analyses data (30). Increased miR-106a expression was prominently associated with malignant clinicopathological features of CC patients, including lymph node metastasis, lymphovascular space invasion and advanced FIGO stage.…”

Section: Discussionsupporting

confidence: 80%

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Zhou

Tao

et al. 2017

Oncology Reports

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Abstract.Increasing evidence has demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies have revealed that miR-106a is abnormally expressed in various cancers. However, its function and underlying mechanism in cervical cancer (CC) remains unknown. In this study, we confirmed that the expression of miR-106a was significantly upregulated in both CC cell lines and tissues by qRT-PCR. The increased expression of miR-106a was obviously associated with adverse prognostic features. Moreover, we demonstrated that miR-106a was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR-106a promoted cell migration, invasion and invasion-related gene expression, while downregulated miR-106a reversed the effect. In addition, miR-106a regulated tissue inhibitor of metalloproteinase (TIMP)2 by directly binding to its 3'-UTR, leading to the indution of the expression of matrix metalloproteinases (MMPs). In clinical samples of CC, miR-106a was inversely correlated with TIMP2, which was downregulated in CC. Alteration of TIMP2 expression at least partially abolished the migration, invasion and MMP expression of miR-106a in CC cells. In conclusion, our data indicated that miR-106a promoted the migration, invasion and MMP expression of CC by targeting TIMP2, and may represent a novel potential therapeutic target and prognostic marker for CC.

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Section: Discussionsupporting

confidence: 80%

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Zhou

Tao

et al. 2017

Oncology Reports

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“…Of interest, we observed some of the same miR clusters altered by HPV16 E6/E7 expression as in studies of cervical cancer (57). HPV16 E6/E7 modulates both tumor-suppressive and oncogenic miR clusters.…”

Section: Discussionsupporting

confidence: 56%

Modulation of microRNA-mRNA Target Pairs by Human Papillomavirus 16 Oncoproteins

Harden

Prasad

Griffiths

et al. 2017

mBio

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The E6 and E7 proteins are the major oncogenic drivers encoded by high-risk human papillomaviruses (HPVs). While many aspects of the transforming activities of these proteins have been extensively studied, there are fewer studies that have investigated how HPV E6/E7 expression affects the expression of cellular noncoding RNAs. The goal of our study was to investigate HPV16 E6/E7 modulation of cellular microRNA (miR) levels and to determine the potential consequences for cellular gene expression. We performed deep sequencing of small and large cellular RNAs in primary undifferentiated cultures of human foreskin keratinocytes (HFKs) with stable expression of HPV16 E6/E7 or a control vector. After integration of the two data sets, we identified 51 differentially expressed cellular miRs associated with the modulation of 1,456 potential target mRNAs in HPV16 E6/E7-expressing HFKs. We discovered that the degree of differential miR expression in HFKs expressing HPV16 E6/E7 was not necessarily predictive of the number of corresponding mRNA targets or the potential impact on gene expression. Additional analyses of the identified miR-mRNA pairs suggest modulation of specific biological activities and biochemical pathways. Overall, our study supports the model that perturbation of cellular miR expression by HPV16 E6/E7 importantly contributes to the rewiring of cellular regulatory circuits by the high-risk HPV E6 and E7 proteins that contribute to oncogenic transformation.

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“…Upregulation of oncomiRs and downregulation of anti‐oncomiRs by miRNA clusters helps the cells to acquire cancer hallmarks. Downregulation of miR‐99 (a member of miR‐let‐7c/99a), miR‐99b/125a and miR‐100/let‐7a‐2 can induce Homeobox A cluster 1 (HOXA1) and tribbles pseudokinase 2 (TRIB2) expression leading to MAPK pathway activation via mitogen‐activated protein kinase kinase 1 (MEK1), facilitating proliferation, migration and invasion (Servín‐González et al, ). Similarly, overexpression of miR‐17/92 and miR‐106a/363, reported to target PTEN and activate PI3K, results in enhanced cell survival, proliferation, migration and invasion.…”

Section: Oncogenic and Tumour‐suppressor Mirna Clustersmentioning

confidence: 99%

Clustered miRNAs and their role in biological functions and diseases

et al. 2018

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MicroRNAs (miRNAs) are endogenous, small non-coding RNAs known to regulate expression of protein-coding genes. A large proportion of miRNAs are highly conserved, localized as clusters in the genome, transcribed together from physically adjacent miRNAs and show similar expression profiles. Since a single miRNA can target multiple genes and miRNA clusters contain multiple miRNAs, it is important to understand their regulation, effects and various biological functions. Like protein-coding genes, miRNA clusters are also regulated by genetic and epigenetic events. These clusters can potentially regulate every aspect of cellular function including growth, proliferation, differentiation, development, metabolism, infection, immunity, cell death, organellar biogenesis, messenger signalling, DNA repair and self-renewal, among others. Dysregulation of miRNA clusters leading to altered biological functions is key to the pathogenesis of many diseases including carcinogenesis. Here, we review recent advances in miRNA cluster research and discuss their regulation and biological functions in pathological conditions.

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Families of microRNAs Expressed in Clusters Regulate Cell Signaling in Cervical Cancer

Cited by 42 publications

References 73 publications

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Modulation of microRNA-mRNA Target Pairs by Human Papillomavirus 16 Oncoproteins

Clustered miRNAs and their role in biological functions and diseases

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