MicroRNA Expression Profiling of Oral Carcinoma Identifies New Markers of Tumor Progression

Scapoli, Luca; Palmieri, Annalisa; Muzio, Lorenzo Lo; Pezzetti, Furio; Rubini, Corrado; Girardi, Ambra; Farinella, F.; Mazzotta, Marco; Carinci, Francesco

doi:10.1177/039463201002300427

Cited by 218 publications

(173 citation statements)

References 26 publications

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“…In this study, we showed that RASSF5 expression was significantly decreased in oral cancer tissues, consistent with results of a previous study showing down-regulation of RASSF5 expression in 54 cases of head and neck cancer patients, including oral cancer (Steinmann et al, 2009). Moreover, we also observed elevated expression levels of miR-214 in oral cancer tissues, consistent with another study (Scapoli et al, 2010). Unsurprisingly, miR-214 levels were reported to be significantly elevated in cisplatin resistant tongue squamous carcinoma cell line Tca/cisplatin compared to those in cisplatin sensitive Tca8113, indicating the role of miR-214 in tumor promotion in oral cancer (Yu et al, 2010).…”

Section: Discussionsupporting

confidence: 91%

“…MiRNAs have been receiving increasing attention for their role in oral cancer (Manikandan et al, 2016). MiR-214 levels were revealed to be up-regulated in oral cancer tissues, indicating that miR-214 might be an oncogene involved in oral cancer (Scapoli et al, 2010). Furthermore, bioinformatics analysis demonstrated that miR-214 could bind to the 3'-UTR of RASSF5.…”

Section: Introductionmentioning

confidence: 99%

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MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

Yin

Chen

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Ras association domain family member 5 (RASSF5), a member of the Ras association domain family, induces cell apoptosis by phosphorylating FOXO3a, which triggers target gene BIM (proapoptotic factor) activation. MiR-214 is overexpressed in oral cancer tissue, indicating its possible involvement in oral cancer pathogenesis. Bioinformatics analysis has revealed a complimentary sequence between miR-214 and the 3'-UTR of RASSF5 mRNA. However, whether miR-124 regulates RASSF5 in oral cancer remains poorly understood. We aimed to investigate the role of miR-214 in RASSF5 expression regulation in oral cancer. Tumor and paracarcinoma tissues were obtained from 48 oral cancer patients to examine miR-214 and RASSF5 expression. The relationship between miR-214 and RASSF5 was investigated by dual luciferase reporter gene assay. Oral cancer KB cells were cultured in vitro and divided into inhibitor NC, miR-214 inhibitor, Scramble-pMD18, RASSF5-pMD18, and miR-214 inhibitor + RASSF5-pMD18 groups. Caspase 3 activity, cell apoptosis, and total protein expression were measured by spectrophotometry, flow cytometry, and western blot, respectively. MiR-214 expression was significantly increased, while that of RASSF5 decreased in oral cancer tumor tissues compared to paracarcinoma tissues. Luciferase assay showed that miR-214 suppressed RASSF5 expression by targeting its 3'-UTR. Down-regulation of miR-214 and/or enhancement of RASSF5 expression markedly increased FOXO3a phosphorylation, BIM expression, caspase 3 activity, and apoptosis. In conclusion, miR-214 expression was elevated and RASSF5 was down-regulated in oral cancer. Moreover, miR-214 regulated KB cell apoptosis through targeted inhibition of RASSF5 expression, FOXO3a phosphorylation, and BIM expression, suggesting its possible application as a novel therapeutic oral cancer target.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

Yin

Chen

et al. 2017

Genet. Mol. Res.

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“…However, decreased miR-132 expression has been observed in osteosarcoma (26) and liver cancer (27). Increased miR-212 expression was reported in oral squamous cell carcinoma (28) and colorectal carcinoma (23), and miR-212 has been shown to be downregulated in gastric cancer (29), NSCLC (30) and head and neck squamous cell carcinoma (31). The different levels of expression of these miRNAs in various cancers indicate that they may exert diverse functions in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells

et al. 2014

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Abstract. Lung cancer is the leading cause of cancer-related mortality worldwide. microRNAs (miRNAs) are small posttranscriptional regulatory non-coding RNAs that function as oncogenes or tumor suppressors in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the progression of human lung cancer, which is the leading cause of cancer-related deaths worldwide. In the present study, we found that upregulation of the miR-212/132 cluster significantly suppressed the growth and focus formation of A549 and H1299 cells. Moreover, forced expression of this cluster conferred radiosensitivity and inhibited the migration of lung cancer cells, whereas downregulation of miR-212/132 reversed the above effects. Furthermore, miR-212/132 overexpression induced cell cycle arrest at the G1/S phase transition of the lung cancer cells, and inhibition of miR-132 and miR-212 abrogated this arrest. In addition, miR-212/132 overexpression increased the percentage of cells undergoing apoptosis. Cells transfected with the miR-212/132 cluster exhibited upregulated p21 expression and reduced cyclin D1 expression. Conversely, cells transfected with the miR-212/132 inhibitor showed reduced expression of p21 and upregulated expression of cyclin D1, suggesting that miR-212/132 may mediate proliferation and cell cycle arrest through p21 and cyclin D1. Our study provides insight into the biological function of the miR-212/132 cluster in lung cancer. The present study may provide a potential therapeutic target for the treatment of lung cancer.

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“…Chronic inflammation increases production of inflammatory cytokines and reactive oxygen species and DNA damage, and results in development and progression of carcinomas (Meira et al, 2008). Oral carcinoma cells upregulate the E-cadherin-targeting miR-92 (Scapoli et al, 2010). Although expression of miR-200 in OSCCs is not known at present, nasopharyngeal carcinomas downregulate it which destabilizes ZEB1/2 mRNA (Chen et al, 2009).…”

Section: Loss Of E-cadherin Expression In Oral Squamous Cell Carcinomasmentioning

confidence: 99%

Cadherin Expression and Progression of Squamous Cell Carcinomas of the Oral Cavity

Imai¹,

Maeda²,

Chiba³

2012

Squamous Cell Carcinoma

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MicroRNA Expression Profiling of Oral Carcinoma Identifies New Markers of Tumor Progression

Cited by 218 publications

References 26 publications

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

Upregulation of the miR-212/132 cluster suppresses proliferation of human lung cancer cells

Cadherin Expression and Progression of Squamous Cell Carcinomas of the Oral Cavity

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