Assessment of MicroRNA-15a and MicroRNA-16-1 Salivary Level in Oral Squamous Cell Carcinoma Patients

MicroRNA ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Soheila Manifar ◽  
Maryam Koopaie ◽  
Shahab Shokouhi Lahiji

Background: Squamous Cell Carcinoma (SCC) includes more than 90% of malignancies of the oral cavity. Early diagnosis could effectively improve patients' quality of life and treatment outcomes of oral cancers. MicroRNAs as non-encoding genes have great potential to initiate or suppress cancer progression. Recent studies have shown that disruption of micro-RNA regulation is a common occurrence in cancers. Objective: This study set out to evaluate the expression of microRNA-15a (miR-15a) and microRNA-16-1 (miR-16-1) in the saliva of Oral Squamous Cell Carcinoma (OSCC) patients in comparison with a healthy control group. Methods: This case-control study was performed on fifteen patients with OSCC and fifteen healthy volunteers as the control group. A 5 ml of non-stimulating whole saliva was collected by spitting method from patients and controls and stored at -70oC. The expression of miR-15a and miR-16-1 was investigated using quantitative Reverse-Transcription Polymerase Chain Reaction (RT-qPCR). Results: MiR-15a and miR-16-1 were downregulated in OSCC patients compared with the control group (p<0.001). The sensitivity of miR-15a and miR-16-1 in differentiating OSCC patients from healthy individuals was 93.3% and 86.67%, respectively, and their specificity was 86.67% and 92.33%, respectively. The diagnostic accuracy of miR-15a was 90%, and miR-16-1 was 93.3%. Conclusion: The present study showed a decrease in the relative expression of miR-15a and miR-16-1 in OSCC patients compared with healthy individuals. It is probable to introduce salivary values of miR-15a and miR-16-1 as a non-invasive tool for early detection of OSCC. Decreased expression of miR-15a and miR-16-1 in OSCC indicates the possible effective role of these genes in OSCC etiopathogenesis.

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ling Mao ◽  
Xiaoweng Wu ◽  
Zhengpeng Gong ◽  
Ming Yu ◽  
Zhi Huang

Abstract Background/objective Accumulated evidence has demonstrated that aerobic glycolysis serves as a regulator of tumor cell growth, invasion, and angiogenesis. Herein, we explored the role of protein disulfide isomerase family 6 (PDIA6) in the aerobic glycolysis and the progression of oral squamous cell carcinoma (OSCC). Methods The expression pattern of PDIA6 in OSCC tissues was determined by qPCR and western blotting. Lentivirus and small interfering RNAs (siRNAs) were introduced into cells to upregulate and downregulate PDIA6 expression. CCK-8, flow cytometry, transwell, and xenotransplantation models were applied to detect cell proliferation, apoptosis, migration, invasion, and tumorigenesis, respectively. Results A high expression pattern of PDIA6 was observed in OSCC tissues, which was closely associated with lower overall survival and malignant clinical features in OSCC. Compared with the control group, overexpression of PDIA6 induced significant enhancements in cell growth, migration, invasiveness, and tumorigenesis and decreased cell apoptosis, while knockdown of PDIA6 caused opposite results. In addition, overexpression of PDIA6 increased glucose consumption, lactate production, and ATP level in OSCC cells. Conclusion This study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted aerobic glycolysis and OSCC progression.


2020 ◽  
Vol 31 (6) ◽  
pp. 634-639
Author(s):  
Shaimaa Ali Hamouda Ali El Basuony ◽  
Reham S. Hamed

Abstract Micro-RNA-221(miR-221) is one of oncogenic miRNAs that plays a vital role in the development and progression of oral cancers. The aim of this study is to introduce a new gene therapy for oral squamous cell carcinoma by blocking the expression of oncogenic miR-221 by its inhibitor. The present work was performed on squamous cell carcinoma cell line SCC-25 and anti-miR-221 was delivered to the cells using an ultrasound micro bubbles. Assessment of the effect of miR-221 inhibitor on SCC-25 cells was done using MTT assay, cell cycle analysis and apoptosis detection. In addition, reverse transcription-polymerase chain reaction was also used to detect the expression -miR-221 and its target genes. Using ANOVA, statistical analysis of the results showed significant inhibition of cell viability with and induction of cell apoptosis of SCC-25 cell line after transfection. Moreover, the expression of miR-221, Epidermal growth factor receptor (EGFR) and CDKNIB/p27 were downregulated without significant difference. Transfection of SCC-25 by inhibitor of miR-221 resulting in blockage of its expression leading to arresting of tumor growth. These results proved the effective role of micro-RNA inhibitors as novel therapeutic agent for oral cancers.


2021 ◽  
Vol 15 (10) ◽  
pp. 2666-2669
Author(s):  
Fiza Shafiq ◽  
Abbas Saleem Khan ◽  
Sajjad Ahmad ◽  
Malik Arshman Khan ◽  
Sikandar Javed , Bajwa ◽  
...  

Background: Oral cancer represents a significant component of the global cancer burden. It develops as a result of multiple risk factors. The main histological form of oral cancer is oral squamous cell carcinoma (OSCC). The disintegration of the extracellular matrix (ECM) is one of the key hallmarks of cancer progression, which stimulates the invasion of tumoral cells into the neighbouring tissue. Matrix metalloproteinases-9 (MMP-9) can degrade different elements of the ECM and basement membrane. Methods: A total of 35 histologically diagnosed cases of OSCC (n=25) and healthy individuals (n=10) as control were included. Immunohistochemical staining was performed on all cases. The results were analysed using SPSS version 20. Results: Increased expression of MMP-9 was observed in OSCC cases (n=23/25; 92%) as compared to healthy individuals. Statistically, a significant relation was observed while comparing the grade of staining intensity and MMP-9 expression among OSCC cases (p=0.001). Conclusion: The present study is planned to assess the immunohistochemical expression of MMP-9 in diagnosed cases of OSCC and healthy individuals. Increased expression of MMP-9 was observed in OSCC as compared to healthy individuals. Evaluation of MMP-9 could be of clinical importance in OSCC and can be used as a diagnostic predictive marker of OSCC. Keywords: Oral squamous cell carcinoma; Matrix Metalloproteinase -9; Immunohistochemistry


2020 ◽  
Author(s):  
Ling Mao ◽  
Xiaoweng Wu ◽  
Zhengpeng Gong ◽  
Ming Yu ◽  
Zhi Huang

Abstract Background/Objective: Accumulated evidence has demonstrated that aerobic glycolysis serves as a regulator of tumor cell growth, invasion and angiogenesis. Herein, we explored the role of protein disulfide isomerase family 6 (PDIA6) in the aerobic glycolysis and the progression of oral squamous cell carcinoma (OSCC). Methods: The expression pattern of PDIA6 in OSCC tissues was determined by qPCR and western blotting. Lentivirus and small interfering RNAs (siRNAs) were introduced into cells to upregulate and downregulate PDIA6 expression. CCK-8, flow cytometry, transwell and xenotransplantation models were applied to detect cell proliferation, apoptosis, migration, invasion and tumorigenesis, respectively. Results: A high expression pattern of PDIA6 was observed in OSCC tissues, which was closely associated with lower overall survival and malignant clinical features in OSCC. Compared with the control group, overexpression of PDIA6 induced significant enhancements in cell growth, migration, invasiveness and tumorigenesis and decreased cell apoptosis, while knockdown of PDIA6 caused opposite results. In addition, overexpression of PDIA6 increased glucose consumption, lactate production and ATP level in OSCC cells.Conclusion: This study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted OSCC progression and aerobic glycolysis.


2015 ◽  
Vol 35 (3) ◽  
Author(s):  
Wei-Peng Jiang ◽  
Zhen Wang ◽  
Li-Xin Xu ◽  
Xin Peng ◽  
Feng Chen

Whole saliva (WS) was used for diagnosis of oral squamous cell carcinoma (OSCC); two polypeptides may be used for OSCC diagnosis.


2021 ◽  
Vol 11 (2) ◽  
pp. 308-314
Author(s):  
Zengbo Wu ◽  
Yan Yan ◽  
Xianzhuo Chen ◽  
Yanling Liu ◽  
Dinggen Chen

miR15b and SALL4 are involved in a variety of tumor progression. The roles of miR15b and SALL4 in oral squamous cell carcinoma (OSCC) remains unclear. The tumors and normal mucosa of OSCC patients were collected to detect miR15b and SALL4 level by Real-time PCR and analyze their correlation with OSCC clinicopathological features. Oral cancer Tca8113 cells were separated into control group; miR15b mimics group and miR15b inhibitor group followed by analysis of SALL4 expression, cell survival by MTT assay; cell invasion by Transwell chamber assay, as well as expression of N-cadherin and Vimentin and correlated with TNM stage, tumor volume and metastasis, and positively with differentiation TGF-β by Western blot. miR15b expression was decreased and SALL4 expression was increased in OSCC tumor tissues. miR15b was negatively degree (P < 0.05), whereas, opposite correlation of SALL4 with the above parameters was found (P < 0.05). miR15b and SALL4 were negatively correlated. MiR15b mimics significantly up-regulated MiR15b, decreased SALL4 expression, inhibited Tca8113 cell proliferation and invasion, as well as reduced N-cadherin, Vimentin and TGF-βexpression (P < 0.05). Opposite results were found in MiR15b inhibitor group. MiR15b expression is decreased and SALL 4 is increased in OSCC tumor tissues. MiR15b and SALL4 is closely related to OSCC clinicopathological features. MiR15b regulates the expression of EMT-related genes and TGF-β, thereby altering the proliferation and invasion of OSCC cells.


Author(s):  
Г.М. Тугузбаева ◽  
В.Н. Павлов ◽  
Д.А. Еникеев

При плоскоклеточном раке полости рта основной причиной летальных исходов является метастазирование в регионарные лимфатические узлы. Злокачественный рост и формирование метастазов напрямую зависят от степени кровоснабжения первичного очага новообразования. Известно, что по мере прогрессирования опухолевый процесс сопровождается нарушением сбалансированной в норме системы регуляции ангиогенеза с превалированием уровня ангиогенных стимуляторов над ингибиторами. В связи с этим, использование антиангиогенных средств является патофизиологически обоснованным методом борьбы со злокачественным ростом. В обзоре обсуждаются данные доклинических исследований участия эндостатина, природного ингибитора ангиогенеза, в процессах подавления прогрессии и метастазирования плоскоклеточного рака челюстно-лицевой области. Проанализированы патогенетические механизмы ингибирования эндостатином опухолевого роста в экспериментальных моделях рака полости рта. Эндостатин можно рассматривать в качестве потенциального противоопухолевого средства для лечения данной нозологии. The main reason for cancer-associated mortality in patients with oral squamous cell carcinoma is metastatic spread to regional lymph nodes. It is known that the processes of malignant growth and metastasis are highly dependent on blood supply to the primary cancerous focus. The development of malignancy is accompanied by failure of the normally well-balanced system of angiogenesis regulation with prevalence of proangiogenic factors over inhibitors. Therefore, the use of angiogenic inhibitors is a pathophysiologically justified method aimed at suppression of cancer progression. This review presents reports of experimental studies on the role of endostatin, a natural inhibitor of angiogenesis, in processes of tumour shrinkage in squamous cell carcinoma of the maxillofacial region. The authors analysed pathogenic mechanisms of the anticancer effects exhibited by endostatin in preclinical models of oral malignancy. Endostatin can be regarded as a potential antitumor agent for the treatment of oral squamous cell carcinoma.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sophia Mentel ◽  
Kathleen Gallo ◽  
Oliver Wagendorf ◽  
Robert Preissner ◽  
Susanne Nahles ◽  
...  

Abstract Background The aim of this study was to evaluate the possibility of breath testing as a method of cancer detection in patients with oral squamous cell carcinoma (OSCC). Methods Breath analysis was performed in 35 OSCC patients prior to surgery. In 22 patients, a subsequent breath test was carried out after surgery. Fifty healthy subjects were evaluated in the control group. Breath sampling was standardized regarding location and patient preparation. All analyses were performed using gas chromatography coupled with ion mobility spectrometry and machine learning. Results Differences in imaging as well as in pre- and postoperative findings of OSCC patients and healthy participants were observed. Specific volatile organic compound signatures were found in OSCC patients. Samples from patients and healthy individuals could be correctly assigned using machine learning with an average accuracy of 86–90%. Conclusions Breath analysis to determine OSCC in patients is promising, and the identification of patterns and the implementation of machine learning require further assessment and optimization. Larger prospective studies are required to use the full potential of machine learning to identify disease signatures in breath volatiles.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaofeng Qi ◽  
Wengguang Xu ◽  
Junqi Xie ◽  
Yufeng Wang ◽  
Shengwei Han ◽  
...  

Abstract Resistance towards chemotherapy is a common complication in treatment of oral cancers, which leads to treatment failure and poor outcome. In recent years, a growing body of evidence has shown that tumour hypoxia significantly contributes to chemoresistance. Metformin, a widely used oral hypoglycaemic drug, can reportedly potentiate the efficacy of chemotherapeutic drugs in various cancers; however, the underlying mechanisms are intricate and have not been fully understood. In this study, we explored the role of metformin in chemosensitivity of oral squamous cell carcinoma cells (OSCC) to cisplatin both in vitro and in vivo, and attempted to elucidate its possible underlying mechanisms. Encouragingly, we found that metformin synergistically enhanced cisplatin cytotoxicity and reversed the chemoresistance to certain extent. This mechanism could likely be related with inhibition of the NF-κB/HIF-1α signal axis and lead to the downregulation of hypoxia-regulated genes products. Therefore, metformin could serve as a chemosensitiser for cisplatin-based regimens for OSCC, thereby providing a theoretical basis for future use in the treatment of oral cancers.


2018 ◽  
Vol 49 (4) ◽  
pp. 1329-1341 ◽  
Author(s):  
Nan Li ◽  
Chuan-Chuan Nan ◽  
Xue-Yun Zhong ◽  
Jun-Quan Weng ◽  
Hai-Dong Fan ◽  
...  

Background/Aims: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. Methods: miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. Results: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. Conclusion: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.


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