scholarly journals The Crossroads of Periodontitis and Oral Squamous Cell Carcinoma: Immune Implications and Tumor Promoting Capacities

2021 ◽  
Vol 1 ◽  
Author(s):  
Omnia Elebyary ◽  
Abdelahhad Barbour ◽  
Noah Fine ◽  
Howard C. Tenenbaum ◽  
Michael Glogauer
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Immune Escape ◽  
Inflammatory Responses ◽  
Gingival Tissue ◽  
Local Inflammatory Response

Periodontitis (PD) is increasingly considered to interact with and promote a number of inflammatory diseases, including cancer. In the case of oral squamous cell carcinoma (OSCC) the local inflammatory response associated with PD is capable of triggering altered cellular events that can promote cancer cell invasion and proliferation of existing primary oral carcinomas as well as supporting the seeding of metastatic tumor cells into the gingival tissue giving rise to secondary tumors. Both the immune and stromal components of the periodontium exhibit phenotypic alterations and functional differences during PD that result in a microenvironment that favors cancer progression. The inflammatory milieu in PD is ideal for cancer cell seeding, migration, proliferation and immune escape. Understanding the interactions governing this attenuated anti-tumor immune response is vital to unveil unexplored preventive or therapeutic possibilities. Here we review the many commonalities between the oral-inflammatory microenvironment in PD and oral-inflammatory responses that are associated with OSCC progression, and how these conditions can act to promote and sustain the hallmarks of cancer.

scholarly journals PDIA6 contributes to aerobic glycolysis and cancer progression in oral squamous cell carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ling Mao ◽  
Xiaoweng Wu ◽  
Zhengpeng Gong ◽  
Ming Yu ◽  
Zhi Huang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Growth ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Expression Pattern ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Aerobic Glycolysis ◽  
Lactate Production ◽  
Control Group

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.

scholarly journals Analysis of the anticancer effect of endostatin on oral squamous cell carcinoma based on results of experimental studies

2020 ◽  
pp. 134-139
Author(s):  
Г.М. Тугузбаева ◽  
В.Н. Павлов ◽  
Д.А. Еникеев
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Experimental Studies ◽  
Antitumor Agent ◽  
Regional Lymph Nodes ◽  
Tumour Shrinkage ◽  
Oral Malignancy

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.

scholarly journals NLRP3 Inflammasome Inhibitor BAY-117082 Reduces Oral Squamous Cell Carcinoma Progression

2021 ◽  
Vol 22 (20) ◽  
pp. 11108
Author(s):  
Sarah Adriana Scuderi ◽  
Giovanna Casili ◽  
Rossella Basilotta ◽  
Marika Lanza ◽  
Alessia Filippone ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Cancer ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Nlrp3 Inflammasome ◽  
P53 Expression

Oral cancer is one of the most common human malignancies, and its incidence is increasing worldwide. In particular, oral squamous cell carcinoma (OSCC) is characterized by high rates of proliferation, invasiveness, and metastasis. Currently, standard treatment for OSCC includes surgical removal, chemotherapy, and radiotherapy; however, the survival rate of patients with OSCC remains low, thus new therapies are needed. It has been proven that excessive NLRP3 inflammasome activation and apoptosis alteration may contribute to oral cancer progression. This study aimed to investigate the effect of BAY-117082, an NLRP3 inflammasome inhibitor, in an in vitro and in vivo xenograft model of oral cancer. In vitro results revealed that BAY-117082 at concentrations of 5, 10, and 30 µM was able to reduce OSCC cell viability. BAY-117082 at higher concentrations significantly reduced NLRP3, ASC, caspase-1, IL-1β, and IL-18 expression. Moreover, Bax, Bad, and p53 expression were increased, whereas Bcl-2 expression was reduced. Furthermore, the in vivo study demonstrated that BAY-117082 at doses of 2.5 and 5 mg/kg significantly decreased subcutaneous tumor mass, and also reduced NLRP3 inflammasome pathway activation. Therefore, based on these results, the use of BAY-117082 could be considered a promising strategy to counteract oral cancer progression, thanks its ability to modulate the NLRP3 inflammasome and apoptosis pathways.

scholarly journals Overexpression of Stathmin in Oral Squamous Cell Carcinoma, its Association with Histomorphological Features and Pathological Staging

2021 ◽  
Author(s):  
Nabanita Barma ◽  
Gopinath Barui ◽  
Anadi Roy Chowdhury
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Tertiary Care ◽  
Clinicopathological Parameters ◽  
Pathological Staging ◽  
Potential Biomarker ◽  
Tobacco Chewing

Introduction: Stathmin, one of the most important intracellular phosphoprotein that plays the vital role in the regulation of cell cycle and cell proliferation. It acts by disassembly of Microtubules (MT) that helps in the formation of mitotic spindle. It is overexpressed in various human cancers. Aim: To investigate the expression status of stathmin and its relation with clinicopathologic significance in Oral Squamous Cell Carcinoma (OSCC) and its association with age, sex, tobacco chewing, histomorphological features and pathological staging. Materials and Methods: A descriptive and observational study in cross-sectional design was conducted in a tertiary care centre of Kolkata, West Bengal, India, from January 2020 to March 2020 in the Department of Pathology of RG Kar Medical College and Hospital in collaboration with Department of Oto-Rhino-Laryngology of the same institute. Stathmin expression was assessed by immunohistochemistry (IHC) in 28 OSCC cases. The association between stathmin expression and clinicopathological parameters like age, sex, tobacco chewing, tumour site, histomorphological type, Tumor Nodes Metastases (TNM) stage and Worst Pattern Of Invasion (WPOI) were evaluated on the basis of Chi-square test and Fisher’s-exact test (software Statistical Package for the Social Sciences (SPSS) V 25.0). Results: Stathmin was overexpressed in 18 cases out of 28 cases of OSCC. In this study a positive association was observed between stathmin expression and age group, history of tobacco chewing, advanced T stage, advanced pTNM staging and WPOI of OSCC. Conclusion: The study suggests that overexpression of stathmin could contribute to cancer progression. There is a higher likelihood that stathmin may be used as a potential biomarker as well as therapeutic target for OSCC.

scholarly journals The Role of Sonic Hedgehog Signaling in the Tumor Microenvironment of Oral Squamous Cell Carcinoma

2019 ◽  
Vol 20 (22) ◽  
pp. 5779 ◽  
Author(s):  
Kiyofumi Takabatake ◽  
Tsuyoshi Shimo ◽  
Jun Murakami ◽  
Chang Anqi ◽  
Hotaka Kawai ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Microenvironment ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Sonic Hedgehog ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Smooth Muscle Actin ◽  
Shh Pathway

Sonic hedgehog (SHH) and its signaling have been identified in several human cancers, and increased levels of SHH expression appear to correlate with cancer progression. However, the role of SHH in the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC) is still unclear. No studies have compared the expression of SHH in different subtypes of OSCC and focused on the relationship between the tumor parenchyma and stroma. In this study, we analyzed SHH and expression of its receptor, Patched-1 (PTCH), in the TME of different subtypes of OSCC. Fifteen endophytic-type cases (ED type) and 15 exophytic-type cases (EX type) of OSCC were used. H&E staining, immunohistochemistry (IHC), double IHC, and double-fluorescent IHC were performed on these samples. ED-type parenchyma more strongly expressed both SHH and PTCH than EX-type parenchyma. In OSCC stroma, CD31-positive cancer blood vessels, CD68- and CD11b-positive macrophages, and α-smooth muscle actin-positive cancer-associated fibroblasts partially expressed PTCH. On the other hand, in EX-type stroma, almost no double-positive cells were observed. These results suggest that autocrine effects of SHH induce cancer invasion, and paracrine effects of SHH govern parenchyma-stromal interactions of OSCC. The role of the SHH pathway is to promote growth and invasion.

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