MicroRNA-375 as a biomarker for malignant transformation in oral lesions

Harrandah, Amani; Fitzpatrick, Sarah; Smith, Molly Housley; Wang, Dunrui; Cohen, Donald M.; Chan, Edward K. L.

doi:10.1016/j.oooo.2016.07.022

Cited by 34 publications

(33 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have emphasized the utility of mir-375 as a biomarker for detection of tongue cancer ( 23 ), malignant transformation of oral lesions ( 39 ), and late stages of oral cancer ( 28 ). Mir-375 has been down-regulated in metastatic oral cancer cell lines compared with less metastatic cells, and mir-375 induced cell migration and invasion by direct targeting the platelet-derived growth factor-A ( PDGF-A ) ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

Zeljić

Jovanović

et al. 2018

Upsala Journal of Medical Sciences

View full text Add to dashboard Cite

AimIt was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients.Material and methodsMeta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis.ResultsAmongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling.ConclusionsThe identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

Zeljić

Jovanović

et al. 2018

Upsala Journal of Medical Sciences

View full text Add to dashboard Cite

show abstract

“…An increasing number of studies have shown that miRNAs played important roles in regulating biological processes, including cell proliferation, metastasis, apoptosis, angiogenesis, and inflammation, in a variety of tumors. 18 , 25 , 26 , 27 , 28 , 29 , 30 Specifically, many studies have indicated that various miRNAs, such as miR-455-5p, 25 miR-211, 31 miR-375, 26 miR-19a/b, 27 miR-204, 32 and miR-187, 33 were related to the development of OSCC. lncRNAs can function as ceRNA sponges for miRNAs to regulate the degradation of miRNA targets.…”

Section: Discussionmentioning

confidence: 99%

The lncRNA PDIA3P Interacts with miR-185-5p to Modulate Oral Squamous Cell Carcinoma Progression by Targeting Cyclin D2

Sun

Zhang

et al. 2017

Molecular Therapy - Nucleic Acids

113

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) are emerging as important regulators during tumorigenesis by serving as competing endogenous RNAs (ceRNAs). In this study, the qRT-PCR results indicated that the lncRNA protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P) was overexpressed in oral squamous cell carcinoma (OSCC) and decreased the survival rate of OSCC patients. CCK-8 and clonal colony formation assays were used to detect the effects of PDIA3P on proliferation. Results revealed that silencing PDIA3P by small interfering RNA (siRNA) inhibited OSCC cell proliferation and repressed tumor growth and reduced the expression of proliferation antigen Ki-67 in vivo. Furthermore, the interaction between PDIA3P and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PDIA3P negatively regulated miR-185-5p in OSCC cells. Simultaneously, we found that silencing PDIA3P by siRNA suppressed proliferation via miR-185-5p in OSCC cells. Moreover, silencing PDIA3P by siRNA inhibited CCND2 protein (no influence on mRNA levels) expression via miR-185-5p in OSCC cells, and CCND2 facilitated cell proliferation of SCC4 and SCC15 cells induced by sh-PDIA3P#1. Therefore, our study demonstrated that PDIA3P may be a therapeutic target for the treatment of OSCC.

show abstract

“…Meanwhile, they showed that miR-375 activates p21 and suppresses telomerase activity by coordinately regulating HPV E6/E7, E6AP, CIP2A, and 14-3-3ζ [26]. Although miR-375 downregulation in oral premalignant lesions is found to be associated with a higher risk of malignant transformation [27], the functions of miR-375 in OSCC development are unclear. Here, we showed that miR-375 is significantly downregulated in OSCC tissues and the level of miR-375 expression could be used as a biomarker to distinguish patients with or without lymph node metastasis.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-375 Inhibits Growth and Enhances Radiosensitivity in Oral Squamous Cell Carcinoma by Targeting Insulin Like Growth Factor 1 Receptor

Zhang

Hou

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: MicroRNAs (miRNAs) have emerged as key players in various human biological processes, including tumorigenesis. Here, we investigated the roles of miR-375 in the pathogenesis of oral squamous cell carcinoma (OSCC). Methods: We performed quantitative real-time PCR (qRT-PCR) to detect miR-375 expression in OSCC tissues and corresponding normal oral epithelial tissues and analyze the correlation of miR-375 expression with OSCC metastasis and patient’s survival. Then, the effects of miR-375 expression on proliferation, cell cycle, apoptosis and radiosensitivity in OSCC cells were determined by using MTT, flow cytometry and clonogenic survival assays. A dual-luciferase reporter assay was performed to test whether miR-375 binds to the 3’-untranslated region (3’-UTR) of target mRNA. Results: The expression level of miR-375 in OSCC tissues was significantly lower than that in normal oral epithelial tissues, and low miR-375 expression was correlated with higher incidence of lymph node metastasis and poor survival of OSCC patients. Upregulation of miR-375 significantly inhibits growth, induces cell cycle arrest in G₀/G₁ phase, increases apoptosis and enhances radiosensitivity in OSCC cells. Analysis of luciferase activity demonstrated that miR-375 binds to the 3’-UTR of insulin like growth factor 1 receptor (IGF-1R). Small interfering RNA (shRNA)-mediated IGF-1R knockdown mimics the effects of miR-375 upregulation, while overexpression of IGF-1R partially reverses those effects in OSCC cells. Conclusion: It was obviously demonstrated that miRNA-375 inhibits growth and enhances radiosensitivity in OSCC cells by targeting IGF-1R, suggesting that miR-375 may be a potential therapeutic target for OSCC patients.

show abstract

MicroRNA-375 as a biomarker for malignant transformation in oral lesions

Cited by 34 publications

References 40 publications

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

The lncRNA PDIA3P Interacts with miR-185-5p to Modulate Oral Squamous Cell Carcinoma Progression by Targeting Cyclin D2

MicroRNA-375 Inhibits Growth and Enhances Radiosensitivity in Oral Squamous Cell Carcinoma by Targeting Insulin Like Growth Factor 1 Receptor

Contact Info

Product

Resources

About