Genomic profile of oral squamous cell carcinomas with an adjacent leukoplakia or with an erythroleukoplakia that evolved after the treatment of primary tumor: A report of two cases

Ribeiro, Ilda Patrícia; Marques, Francisco Batel; Barroso, Leonor; Rodrigues, João; Caramelo, Francisco; Melo, Joana B.; Carreira, Isabel M.

doi:10.3892/mmr.2017.7428

Cited by 13 publications

(11 citation statements)

References 29 publications

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“…The online software programs DIANA, miRDB, miRWalk, and TargetScan were used to predict the potential target genes of miR‐626, and 32 genes were shown as the predicted potential target genes (Figure 2A, Figure ). Eleven dysregulated genes were detected in OSCC tissues or cell lines, as reported by previous studies, including downregulated (RASSF4, 18 RCOR1, 24 DLG2 25 ) and upregulated genes (MEIS2, 26 MTDH, 6 DUSP4, 27 MFAP5, 28 KDM8, 29 NR4A3, 30 EYA4, 31 and FBXL5 32 ). MiRNAs have been widely reported to regulate gene expression by inhibiting translation and/or by inducing degradation of target genes 33 .…”

Section: Resultssupporting

confidence: 79%

Wnt/β‐catenin signaling pathway participates in the effect of miR‐626 on oral squamous cell carcinoma by targeting RASSF4

Cui

Yan

2021

J Oral Pathology Medicine

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Background The role of miR‐626 in oral squamous cell carcinoma (OSCC) was investigated by targeting RASSF4. Methods The miR‐626 and RASSF4 expression was detected in normal oral mucosa or OSCC tissues and OSCC or normal cells. The methylation status of RASSF4 was analyzed using methylation‐specific polymerase chain reaction (PCR). The cytoplasmic/nuclear ratios (C/N ratios) targeted by miR‐626 were examined using microarray, followed by a dual‐luciferase reporter assay. The subcellular localization of RASSF4 and miR‐626 in OSCC cells was determined using RNA fluorescence in situ hybridization (FISH) and immunocytochemistry (ICC), respectively. Ca9‐22 and HSC2 cells were divided into mock, inhibitor NC, miR‐626 inhibitor, scramble, RASSF4 and miR‐626 mimic + RASSF4 groups, and then CCK‐8, Annexin V‐FITC/PI, wound healing, Transwell, qRT‐PCR and western blotting assays were performed. Results OSCC tissues and cells had increased miR‐626 expression and decreased RASSF4 expression. Patients with RASSF4 methylation had lower RASSF4 expression than those without methylation. In addition, a negative correlation between miR‐626 and RASSF4 was found in OSCC tissues, both of which were correlated with the pathological grade, pathological stage, lymph node metastasis and patient prognosis. MiR‐626 targeted RASSF4 in OSCC cells. Overexpressed RASSF4 inhibited the proliferation, invasion, migration and epithelial–mesenchymal transition (EMT) of OSCC cells, promoted cell apoptosis, and blocked the Wnt/β‐Catenin pathway, which was reversed by miR‐626 overexpression. Conclusions Inhibiting miR‐626 can regulate the biological characteristics of OSCC cells, including proliferation, invasion, migration, EMT and apoptosis, by targeting RASSF4, which may be related to the Wnt/β‐Catenin pathway.

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Section: Resultssupporting

confidence: 79%

Wnt/β‐catenin signaling pathway participates in the effect of miR‐626 on oral squamous cell carcinoma by targeting RASSF4

Cui

Yan

2021

J Oral Pathology Medicine

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“…The genomic profiles of two OSCC, one co‐occurring with an OL and the second being followed by an erythroleukoplakia after the primary tumour treatment, were evaluated by aCGH 34 . Both the OL and erythroleukoplakia cases showed more genomic imbalances than the respective invasive tumours 34 . However, the limited number of samples evaluated does not allow any conclusions.…”

Section: Copy Number Alterationsmentioning

confidence: 99%

The genetic basis of oral leukoplakia and its key role in understanding oral carcinogenesis

Guimarães

Diniz

Rogatto

et al. 2020

J Oral Pathology Medicine

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Oral leukoplakia (OL) is the most common oral potentially malignant disorder, with a global prevalence of 2%‐3%, variable malignant transformation rate and incompletely understood aetiology. Considering the subjectivity in oral dysplasia grading, other evaluation methods have been tested as predictors of malignant transformation. DNA ploidy status and loss of heterozygosity signatures have been shown to be good predictive markers of malignant transformation. However, effective markers to predict which lesions will progress to invasive carcinoma and by which mechanisms remain unclear. Recent evidence suggests that dysplasia progression to carcinoma occurs through neutral clonal evolution (i.e. randomly). We focus on the genetic basis of OL, encompassing the gross chromosomal alterations and single‐gene mutations, and discuss such alterations in the context of aetiology, clinical presentation and progression. The deeper we understand the genetic basis of OL, the more we approach a better comprehension of the complex and poorly understood process of oral carcinogenesis.

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“…OL is considered as the most frequently observed premalignant lesion involving the oral cavity [3]. Additionally, at the time of OSCC diagnosis, up to 60% patients have co-incidence of OL [4].…”

Section: Introductionmentioning

confidence: 99%

Prevalence of Oral Leukoplakia in 9954 Central Indian Patients: a Prospective, Cross-sectional Study

Rahangdale

Phulambrikar

Dosi

et al. 2022

Preprint

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Introduction India is one of the leading producers and consumer of tobacco. Additionally, India has one of the highest global prevalence of oral leukoplakia (OL). However, large epidemiological studies from Madhya Pradesh (Central India), the state with maximum consumers of tobacco products in India, are lacking. Objective Thus, we assessed the prevalence of OL among individuals residing in Central India and evaluated its association with age, gender, and history of adverse habits. Methods This was a prospective, cross-sectional study involving 9954 patients visiting the out-patient Department of Oral Medicine and Radiology over a period of 15 months (January 2019 to March 2020). The clinical diagnosis of OL was arrived by exclusion of all the lesions mimicking OL. Univariate and multivariate analyses were performed to assess the association between OL and age, sex, and history of adverse habits. Results The prevalence of OL was 5.6% (557/9954). It was predominant in males (male-to-female ratio=3.9:1) and increased with advancing age. The odds of developing OL was higher among patients aged ≥50 years (OR=1.08; 95%CI: 1.07–1.08, p-value<0.0001), those with history of smoking tobacco (OR=1.32; 95%CI: 1.05–1.68, p-value=0.02), consuming smokeless tobacco (OR=318.60; 95%CI: 101.68–998.30, p-value<0.0001), and alcohol (OR=1.15; 95%CI: 9.0–1.49, p-value=0.269). Females had lower odds of developing OL (OR=0.77; 95%CI: 0.60–0.99, p-value=0.042). Conclusion We observed high prevalence of OL (5.6%). OL was significantly associated with older age, male sex, and tobacco-related adverse habits. While, alcohol consumption may possibly be a risk factor, no statistically significant relation was observed.

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Genomic profile of oral squamous cell carcinomas with an adjacent leukoplakia or with an erythroleukoplakia that evolved after the treatment of primary tumor: A report of two cases

Cited by 13 publications

References 29 publications

Wnt/β‐catenin signaling pathway participates in the effect of miR‐626 on oral squamous cell carcinoma by targeting RASSF4

Wnt/β‐catenin signaling pathway participates in the effect of miR‐626 on oral squamous cell carcinoma by targeting RASSF4

The genetic basis of oral leukoplakia and its key role in understanding oral carcinogenesis

Prevalence of Oral Leukoplakia in 9954 Central Indian Patients: a Prospective, Cross-sectional Study

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