MicroRNAs as prognostic molecular signatures in human head and neck squamous cell carcinoma: A systematic review and meta-analysis

Jamali, Zahra; Aminabadi, Naser Asl; Attaran, Rana; Pournagi-Azar, Fatemeh; Oskouei, Sina Ghertasi; Ahmadpour, Farzin

doi:10.1016/j.oraloncology.2015.01.008

Cited by 129 publications

(128 citation statements)

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“…We here also demonstrated that miR-200c, and miR-203 expressions were significantly correlated with miR-203, and miR-363-3p expressions, respectively, in CD133 + LCa tissue samples. Correlation of those microRNAs expressions supports a recent report, which demonstrated that decreased expressions of miR-200c, miR-363, and miR-203 were associated with poor prognosis in human head and neck squamous cell carcinoma [81]. Besides, coordinated loss of miR-200c and miR-203 has been found to result in enhanced translation of the multiple targets and chronic activation of NF-κB, PI3K-Akt, and Ras-Erk pathways, leading to B cell transformation, which suggest that collaborative actions of multiple miRNAs rather than a single miRNA ensure the robustness of biological processes [82].…”

Section: Discussionsupporting

confidence: 85%

Identification of microRNA profile specific to cancer stem-like cells directly isolated from human larynx cancer specimens

et al. 2016

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BackgroundEmerging evidences proposed that microRNAs are associated with regulation of distinct physio-pathological processes including development of normal stem cells and carcinogenesis. In this study we aimed to investigate microRNA profile of cancer stem-like cells (CSLCs) isolated form freshly resected larynx cancer (LCa) tissue samples.MethodsCD133 positive (CD133+) stem-like cells were isolated from freshly resected LCa tumor specimens. MicroRNA profile of 12 pair of CD133+ and CD133− cells was determined using microRNA microarray and differential expressions of selvected microRNAs were validated by quantitative real time PCR (qRT-PCR).ResultsMicroRNA profiling of CD133+ and CD133− LCa samples with microarray revealed that miR-26b, miR-203, miR-200c, and miR-363-3p were significantly downregulated and miR-1825 was upregulated in CD133+ larynx CSLCs. qRT-PCR analysis in a total of 25 CD133+/CD133− sample pairs confirmed the altered expressions of these five microRNAs. Expressions of miR-26b, miR-200c, and miR-203 were significantly correlated with miR-363-3p, miR-203, and miR-363-3p expressions, respectively. Furthermore, in silico analysis revealed that these microRNAs target both cancer and stem-cell associated signaling pathways.ConclusionsOur results showed that certain microRNAs in CD133+ cells could be used as cancer stem cell markers. Based on these results, we propose that this panel of microRNAs might carry crucial roles in LCa pathogenesis through regulating stem cell properties of tumor cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2863-3) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 85%

Identification of microRNA profile specific to cancer stem-like cells directly isolated from human larynx cancer specimens

et al. 2016

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“…HPGD is a known anti-tumorigenic effecter, and it regulates the tumorigenic actions of Prostaglandin E2 (PGE2) by converts PGE2 to its biologically inactive metabolite, and down-regulation of HPGD has been observed in many human cancer types [47–53]. Since miR-21 is one of the most consistently observed up-regulated microRNA in OTSCC [16, 54], the miR-21-HPGD regulatory module may represents a critical mechanism of regulating PGE2 signaling.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-21 regulates prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cell carcinoma

Chen

Dong

et al. 2016

BMC Cancer

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BackgroundOral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive forms of head and neck/oral cancer (HNOC), and is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. Identifying the deregulation of microRNA-mRNA regulatory modules (MRMs) is crucial for understanding the role of microRNA in OTSCC.MethodsA comprehensive bioinformatics analysis was performed to identify MRMs in HNOC by examining the correlation among differentially expressed microRNA and mRNA profiling datasets and integrating with 12 different sequence-based microRNA target prediction algorithms. Confirmation experiments were performed to further assess the correlation among MRMs using OTSCC patient samples and HNOC cell lines. Functional analyses were performed to validate one of the identified MRMs: miR-21-15-Hydroxyprostaglandin Dehydrogenase (HPGD) regulatory module.ResultsOur bioinformatics analysis revealed 53 MRMs that are deregulated in HNOC. Four high confidence MRMs were further defined by confirmation experiments using OTSCC patient samples and HNOC cell lines, including miR-21-HPGD regulatory module. HPGD is a known anti-tumorigenic effecter, and it regulates the tumorigenic actions of Prostaglandin E2 (PGE2) by converts PGE2 to its biologically inactive metabolite. Ectopic transfection of miR-21 reduced the expression of HPGD in OTSCC cell lines, and the direct targeting of the miR-21 to the HPGD mRNA was confirmed using a luciferase reporter gene assay. The PGE2-mediated upregulation of miR-21 was also confirmed which suggested the existence of a positive feed-forward loop that involves miR-21, HPGD and PGE2 in OTSCC cells that contribute to tumorigenesis.ConclusionsWe identified a number of high-confidence MRMs in OTSCC, including miR-21-HPGD regulatory module, which may play an important role in the miR-21-HPGD-PGE2 feed-forward loop that contributes to tumorigenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2716-0) contains supplementary material, which is available to authorized users.

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“…Down-regulation of let-7d is associated with poor survival, disease recurrence, and distant metastasis in oral cancer (62). Similarly, down-regulation of miR-200c correlates with EMT and loss of E-cadherin (61).…”

Section: Par-2-mediated Nf-b Activation Suppresses Micrornamentioning

confidence: 99%

Protease-activated Receptor-2 (PAR-2)-mediated Nf-κB Activation Suppresses Inflammation-associated Tumor Suppressor MicroRNAs in Oral Squamous Cell Carcinoma

Johnson

Miller

Jiang

et al. 2016

Journal of Biological Chemistry

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Oral cancer is the sixth most common cause of death from cancer with an estimated 400,000 deaths worldwide and a low (50%) 5-year survival rate. The most common form of oral cancer is oral squamous cell carcinoma (OSCC). OSCC is highly inflammatory and invasive, and the degree of inflammation correlates with tumor aggressiveness. The G protein-coupled receptor protease-activated receptor-2 (PAR-2) plays a key role in inflammation. PAR-2 is activated via proteolytic cleavage by trypsin-like serine proteases, including kallikrein-5 (KLK5), or by treatment with activating peptides. PAR-2 activation induces G protein-␣-mediated signaling, mobilizing intracellular calcium and Nf-B signaling, leading to the increased expression of pro-inflammatory mRNAs. Little is known, however, about PAR-2 regulation of inflammation-related microRNAs. Here, we assess PAR-2 expression and function in OSCC cell lines and tissues. Stimulation of PAR-2 activates Nf-B signaling, resulting in RelA nuclear translocation and enhanced expression of pro-inflammatory mRNAs. Concomitantly, suppression of the anti-inflammatory tumor suppressor microRNAs let-7d, miR-23b, and miR-200c was observed following PAR-2 stimulation. Analysis of orthotopic oral tumors generated by cells with reduced KLK5 expression showed smaller, less aggressive lesions with reduced inflammatory infiltrate relative to tumors generated by KLK5-expressing control cells. Together, these data support a model wherein KLK5-mediated PAR-2 activation regulates the expression of inflammation-associated mRNAs and microRNAs, thereby modulating progression of oral tumors. Squamous cell carcinoma of the oral cavity (OSCC)2 is a highly inflammatory disease that ranks as the 6th most frequently diagnosed cancer worldwide, with a poor 5-year survival rate of about 50% (1). Early diagnosis of OSCC is challenging, predominantly because early oral cancers and premalignant lesions are often subtle and asymptomatic. Although many patients present for diagnosis with stage III or IV disease, premalignant lesions in the oral mucosa often precede invasive OSCC (2). Furthermore, unlike most solid tumors that are monoclonal in origin, multiple distinct foci of dysplastic cells may be present in the oral mucosa. These epithelial dysplasia are categorized as mild, moderate, severe, or carcinoma in situ based on the histologic abnormalities present in the oral epithelium (3). Studies show that ϳ12-36% of epithelial dysplasia progress to carcinoma (4, 5); however, current approaches do not enable accurate identification of premalignant lesions likely to undergo malignant transformation.The link between inflammation and cancer is now well established, and inflammatory mediators are present in the microenvironment of virtually all solid tumors (6 -10). Many studies have associated proteinase-activated receptor-2 (PAR-2) with both inflammation and tumor progression (11-15); however, the expression of PAR-2 in OSCC has not been evaluated. PAR-2 is a G protein-coupled receptor that is activated by trypsin-...

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MicroRNAs as prognostic molecular signatures in human head and neck squamous cell carcinoma: A systematic review and meta-analysis

Cited by 129 publications

References 53 publications

Identification of microRNA profile specific to cancer stem-like cells directly isolated from human larynx cancer specimens

Identification of microRNA profile specific to cancer stem-like cells directly isolated from human larynx cancer specimens

MicroRNA-21 regulates prostaglandin E2 signaling pathway by targeting 15-hydroxyprostaglandin dehydrogenase in tongue squamous cell carcinoma

Protease-activated Receptor-2 (PAR-2)-mediated Nf-κB Activation Suppresses Inflammation-associated Tumor Suppressor MicroRNAs in Oral Squamous Cell Carcinoma

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