mi<scp>RNA</scp> expression profile of mucoepidermoid carcinoma

Binmadi, Nada O.; Basile, John R.; Pérez, Paola; Gallo, Alessia; Tandon, Mayank; Elias, Wael Y; Jang, Shyh‐Ing; Alevizos, Ilias

doi:10.1111/odi.12800

Cited by 22 publications

(25 citation statements)

References 24 publications

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“…Among the increased miRNAs in mucoepidermoid carcinoma, miR‐302a shows the most pronounced change . In OC, miR‐302a downregulates SDC1 to increase tumor cell apoptosis .…”

Section: Functions and Mechanisms Of Mir‐302 Cluster In Tumor Developmentioning

confidence: 99%

Application of the microRNA‐302/367 cluster in cancer therapy

Liu

Wang

et al. 2020

Cancer Science

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This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. , glycogen synthase kinase-3β; HCC, hepatocellular carcinoma; HECC, human endometrial carcinoma cell; hESC, human embryonic stem cell; IGF-1R, insulin-like growth factor 1 receptor; iPSCs, induced pluripotent stem cells; JNK, c-Jun NH2-terminal kinase; KLF4, Kruppel Like Factor 4; KPNA2, NF-κB-inducing kinase and karyopherin α2; LATS2, large tumor suppressor kinase 2; lncRNA, long noncoding RNA; LSCC, laryngeal squamous cell carcinoma; Mcl-1, myeloid cell leukemia sequence 1; MIAT, myocardial infarction-associated transcript; miRNA, microRNA; mirPS, miRNA-induced pluripotent stem; MTDH, metadherin; ncRNA, noncoding RNA; NK, natural killer; Notch4, notch receptor 4; NR2F2, nuclear receptor subfamily 2 group F member 2; OC, ovarian cancer; OCT, organic cation/carnitine transporter; PCa, prostate cancer; P-gp, P-glycoprotein; PRP-1, proline-rich polypeptide 1; RACK1, receptor for activated C-kinase 1; S1pr1, sphingosine-1-phosphate receptor 1; SDC1, syndecan 1; SDF1, stromal cell-derived factor 1; SHH, sonic hedgehog; SOX2, SRY-box transcription factor 2; Tcf3, transcription factor 3; SSEA-4, stage-specific embryonic antigen-4; YAP, Yes-associated transcriptional regulator. AbstractAs a novel class of noncoding RNAs, microRNAs (miRNAs) can effectively silence their target genes at the posttranscriptional level. Various biological processes, such as cell proliferation, differentiation, and motility, are regulated by miRNAs. In different diseases and different stages of disease, miRNAs have various expression patterns, which makes them candidate prognostic markers and therapeutic targets.Abnormal miRNA expression has been detected in numerous neoplastic diseases in humans, which indicates the potential role of miRNAs in tumorigenesis. Previous studies have indicated that miRNAs are involved in nearly the entire process of tumor development. MicroRNA-302a, miR-302b, miR-302c, miR-302d, and miR-367 are members of the miR-302/367 cluster that plays various biological roles in diverse neoplastic diseases by targeting different genes. These miRNAs have been implicated in several unique characteristics of cancer, including the evasion of growth suppressors, the sustained activation of proliferative signaling, the evasion of cell death and senescence, and the regulation of angiogenesis, invasion, and metastasis.This review provides a critical overview of miR-302/367 cluster dysregulation and the subsequent effects in cancer and highlights the vast potential of members of this cluster as therapeutic targets and novel biomarkers. K E Y W O R D Sbiological phenomena, cell dedifferentiation, MIRN302, neoplasm, therapy

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“…Among the increased miRNAs in mucoepidermoid carcinoma, miR‐302a shows the most pronounced change . In OC, miR‐302a downregulates SDC1 to increase tumor cell apoptosis .…”

Section: Functions and Mechanisms Of Mir‐302 Cluster In Tumor Developmentioning

confidence: 99%

Application of the microRNA‐302/367 cluster in cancer therapy

Liu

Wang

et al. 2020

Cancer Science

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“…MicroRNAs (miRNAs) are small ncRNAs molecules that control gene expression level after transcription [15]. Accumulating evidence shows that miRNAs represent abnormal expression in many human tumours, such as OS [16], gastric tumour [17] and mucoepidermoid carcinoma [18]. Moreover, miRNAs participate in numerous biological, pathological proceedings, physiological perturbations and disease conditions.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The circular RNA circ-ITCH acts as a tumour suppressor in osteosarcoma via regulating miR-22

Ren

Liu

Zheng

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Osteosarcoma (OS) is the most prevailing primary bone tumour and the third prevalent tumour in children and adolescents. Despite advanced treatments, the survival rate of OS has not been effectively improved. Here, we intended to investigate the functional impacts of circ-ITCH on OS. Methods: Circ-ITCH expression in OS tissues and cells was evaluated utilizing qRT-PCR. Viability and proliferation of MG63 and Saos-2 cells were determined by utilizing CCK-8 assay and BrdU assay. Transwell assay was utilized to investigate migration and invasion. Western blot was utilized to distinguish apoptosis and metastasis-related proteins expression. Sequentially, the above-mentioned parameters were reassessed when up-regulating miR-22. Results: Circ-ITCH was low expressed in OS tissues and cells. Overexpressing circ-ITCH facilitated apoptosis and repressed viability, proliferation, migration and invasion in MG63 and Saos-2 cells. MiR-22 expression was reduced by overexpressing circ-ITCH. The decline of viability, proliferation, migration and invasion made by overexpressing circ-ITCH was alleviated by up-regulating miR-22. Conclusively, circ-ITCH suppressed PTEN/PI3K/AKT and SP-1 pathways via down-regulating miR-22. Conclusion: Circ-ITCH took effects on apoptosis, viability, proliferation, migration and invasion through restraining PTEN/PI3K/AKT and SP-1 pathways via down-regulating miR-22 in MG63 and Saos-2 cells. HIGHLIGHTS 1. Low expression of circ-ITCH is observed in osteosarcoma tissues and cell lines; 2. Overexpression circ-ITCH suppresses miR-22 expression; 3. Circ-ITCH promotes proliferation and represses apoptosis by up-regulating miR-22; 4. Circ-ITCH promotes migration and invasion by up-regulating miR-22; 5. Circ-ITCH activates PTEN/PI3K/AKT and SP-1 pathways by up-regulating miR-22.

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“…Hyper-or hypomethylation of DNA may induce the development of tumors by regulating their components, such as proteins of the extracellular matrix, and it can cause chromosomal instability (Dawson & Kouzarides, 2012;Sharma et al, 2010). Epigenetic alterations, isolated or combined, may be involved in the development and progress of SGT (Aniello et al, 2006;Augello et al, 2006;Binmadi et al, 2018;Daa et al, 2008;Durr et al, 2010;Ge et al, 2011;Guimarães et al, 2016;Hu et al, 2011;Kaira et al, 2013;Ling et al, 2016;Nikolic et al, 2018;Schache et al, 2010;Shao et al, 2011Shao et al, , 2012Stephens et al, 2013;Tan et al, 2014;Wagner et al, 2017;Wang et al, 2015;Williams et al, 2006;Xia et al, 2018Xia et al, , 2013Zhang et al, 2007Zhang et al, , 2014.…”

Section: Dna Me Thyl Ati On In Salivary G L and Tumor Smentioning

confidence: 99%

Epigenetic alterations in salivary gland tumors

et al. 2020

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Despite their rarity compared to other neoplasms, salivary gland tumors (SGTs) are relatively frequent in the context of head and neck tumors (El-Naggar, Chan, Grandis, Takata, & Sootweg, 2017). These lesions comprise a heterogeneous group of benign and malignant neoplasms with significant variability in their microscopic appearance and clinical presentation, and its biological behavior can vary according to the lesion (Fonseca, Sena Filho, Altemani, Speight, & Vargas, 2016). The management of these neoplasms is a challenge due to their unpredictable clinical and biological behavior that may lead to failure in response to treatment (Wagner et al., 2017). Salivary gland tumors represent 5% of all head and neck neoplasms, with an estimated global annual incidence varying from 0.4 to 13.5 cases per 100,000 inhabitants (Fonseca et al., 2012). According to the World Health Organization (WHO) classification of head and neck tumors, there are more than 30 neoplasms recognized (El-Naggar et al., 2017). Mucoepidermoid carcinoma and pleomorphic adenoma are the most frequent malignant and benign neoplasms, respectively (El-Naggar et al., 2017). Several studies have been developed on this topic; however, the etiologic factors are still unknown, although chromosomic translocation, secondary radiation, and chemotherapy may be associated with the development of SGT (El-Naggar et al., 2017). Furthermore, epigenetic alterations have also been suggested as etiological factors, although there are still few studies analyzing its role in SGT (

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miRNA expression profile of mucoepidermoid carcinoma

Abstract: These promising results suggest the need for further studies to establish mir-302a as a marker of invasion and aggressiveness in MEC.

Cited by 22 publications

References 24 publications

Application of the microRNA‐302/367 cluster in cancer therapy

Application of the microRNA‐302/367 cluster in cancer therapy

RETRACTED ARTICLE: The circular RNA circ-ITCH acts as a tumour suppressor in osteosarcoma via regulating miR-22

Epigenetic alterations in salivary gland tumors

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