scholarly journals Immunohistochemical Analysis of the Beclin-1 Expression Predicts the Progression of Oral Squamous Cell Carcinoma

Author(s):  
Ida Barca ◽  
Chiara Mignogna ◽  
Daniela Novembre ◽  
Francesco Ferragina ◽  
Maria Giulia Cristofaro

Background: Autophagy is a cellular process responsible for maintaining homeostasis; a dysregulation of this process is involved in the development and progression of neoplasms. Beclin-1 is one of the major proteins linked to autophagy. However, the data regarding the association between the role of Beclin-1 and the progression of Oral Squamous Cell Carcinoma (OSCC) are rather low. For this reason, the objective of this study is to evaluate, through immunohistochemical techniques, the prognostic role of the expression of Beclin-1 autophagy marker in patients with OSCC. Methods: This is a single-centre retrospective study that includes patients with OSCC admitted to the Maxillofacial Unit of “Magna Graecia” University between January 2019 and September 2020. All the samples obtained from surgery were treated with anti Beclin-1 antibodies and subjected to immunohistochemical methods. Results: A total of 26 samples were analysed and the following variables were evaluated for each: percentage of positive Beclin-1 expression by tumour cells, signal strength of tumour cells, and total score. The variables considered were first normalised according to the D’Agostino and Pearson test, then analysed using the Pearson linear correlation coefficient: a statistically significant correlation was found between the parameters infiltration-intensity (p = 0.0088), infiltration-percent (p = 0.0123), intensity-total score (p = 0.0060). Conclusions: The immunohistochemical evaluation of Beclin-1 revealed a statistically significant correlation between the intensity of the molecule’s expression and a greater degree of infiltration of the neoplasm. Beclin-1 can, therefore, be considered a valid prognostic index of disease.

2020 ◽  
Vol 40 (12) ◽  
pp. 6987-6995
Author(s):  
NORBERT NECKEL ◽  
MARCO MICHAEL ◽  
DANIEL TROELTZSCH ◽  
JONAS WÜSTER ◽  
STEFFEN KOERDT ◽  
...  

2012 ◽  
Vol 6 (2) ◽  
pp. 21 ◽  
Author(s):  
Rashmi Metgud ◽  
Madhusudan Astekar ◽  
Meenal Verma ◽  
Ashish Sharma

The etiology of oral squamous cell carcinoma (OSCC) is complex and involves many factors. The most clearly defined risk factors are smoking and alcohol, which substantially increase the risk of oral SCC. However, despite this clear association, a substantial proportion of patients develop OSCC without exposure to them, emphasizing the role of other risk factors such as genetic susceptibility and oncogenic viruses. Some viruses are strongly associated with OSCC while the association of others is less frequent and may depend on co-factors for their carcinogenic effects. Therefore, the exact role of viruses must be evaluated with care in order to improve the diagnosis and treatment of OSCC.


2014 ◽  
Vol 122 (3) ◽  
pp. 198-201 ◽  
Author(s):  
Annalisa Palmieri ◽  
Francesco Carinci ◽  
Marcella Martinelli ◽  
Furio Pezzetti ◽  
Ambra Girardi ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yilong Ai ◽  
Shiwei Liu ◽  
Hailing Luo ◽  
Siyuan Wu ◽  
Haigang Wei ◽  
...  

N6-Methyladenosine (m6A) modification is one of the commonest chemical modifications in eukaryotic mRNAs, which has essential effects on mRNA translation, splicing, and stability. Currently, there is a rising concern on the regulatory role of m6A in tumorigenesis. As a known component in the m6A methyltransferase complex, METTL3 (methyltransferase-like 3) plays an essential role in m6A methylation. Till now, the functions of METTL3 in oral squamous cell carcinoma (OSCC) and its relative mechanism remain to be explored. In this research, through the GEPIA database, we found that high METTL3 expression has a correlation with poor prognosis of squamous cell carcinoma of head and neck. qRT-PCR displayed that METTL3 was highly expressed in OSCC cells. Functionally, METTL3 knockdown reduced the invasion, migration, and proliferation competence of OSCC cells and attenuated the activation of CD8+ T cells. In contrast, METTL3 overexpression resulted in opposite results. GEPIA, UALCAN, and SRAMP databases, PCR, western blot, and m6A RNA methylation assay confirmed the m6A modification of PRMT5 and PD-L1 mediated by METTL3. In conclusion, our results displayed that METTL3 intensified the metastasis and proliferation of OSCC by modulating the m6A amounts of PRMT5 and PD-L1, suggesting that METTL3 may be a therapeutic target for OSCC patients.


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