scholarly journals Involvement of Fusobacterium Species in Oral Cancer Progression: A Literature Review Including Other Types of Cancer

2020 ◽  
Vol 21 (17) ◽  
pp. 6207 ◽  
Author(s):  
Natsumi Fujiwara ◽  
Naoya Kitamura ◽  
Kaya Yoshida ◽  
Tetsuya Yamamoto ◽  
Kazumi Ozaki ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Progression ◽  
Periodontal Diseases ◽  
Bacterial Species ◽  
Clinical Stage ◽  
Host Cells ◽  
Cancer Development ◽  
Human Teeth ◽  
Mesenchymal Transition ◽  
Fusobacterium Species

Chronic inflammation caused by infections has been suggested to be one of the most important cause of cancers. It has recently been shown that there is correlation between intestinal bacteria and cancer development including metastasis. As over 700 bacterial species exist in an oral cavity, it has been concerning that bacterial infection may cause oral cancer. However, the role of bacteria regarding tumorigenesis of oral cancer remains unclear. Several papers have shown that Fusobacterium species deriving the oral cavities, especially, play a crucial role for the development of colorectal and esophageal cancer. F. nucleatum is a well-known oral bacterium involved in formation of typical dental plaque on human teeth and causing periodontal diseases. The greatest characteristic of F. nucleatum is its ability to adhere to various bacteria and host cells. Interestingly, F. nucleatum is frequently detected in oral cancer tissues. Moreover, detection of F. nucleatum is correlated with the clinical stage of oral cancer. Although the detailed mechanism is still unclear, Fusobacterium species have been suggested to be associated with cell adhesion, tumorigenesis, epithelial-to-mesenchymal transition, inflammasomes, cell cycle, etc. in oral cancer. In this review, we introduce the reports focused on the association of Fusobacterium species with cancer development and progression including oral, esophageal, and colon cancers.

scholarly journals MicroRNA-381—A Key Transcriptional Regulator: Its Biological Function and Clinical Application Prospects in Cancer

2020 ◽  
Vol 10 ◽  
Author(s):  
Xue Zeng ◽  
Zhe Cao ◽  
Wenhao Luo ◽  
Lianfang Zheng ◽  
Taiping Zhang
Keyword(s):  
Prognostic Factor ◽  
Clinical Application ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Stage ◽  
Cancer Development ◽  
Messenger Rnas ◽  
Mesenchymal Transition ◽  
Oncogenic Pathways ◽  
Application Prospects

MicroRNAs (miRNAs) are small non-coding RNA molecules that function by regulating messenger RNAs. Recent studies have shown that miRNAs play important roles in multiple processes of cancer development. MiR-381 is one of the most important miRNAs in cancer progression. MiR-381 is downregulated in some cancers and upregulated in other cancers, including glioma, epithelial sarcoma, and osteosarcoma. MiR-381 regulates epithelial–mesenchymal transition (EMT), chemotherapeutic resistance, radioresistance, and immune responses. Thus, miR-381 participates in tumor initiation, progression, and metastasis. Moreover, miR-381 functions in various oncogenic pathways, including the Wnt/β-catenin, AKT, and p53 pathways. Clinical studies have shown that miR-381 could be considered a biomarker or a novel prognostic factor. Here, we summarize the present studies on the role of miR-381 in cancer development, including its biogenesis and various affected signaling pathways, and its clinical application prospects. MiR-381 expression is associated with tumor stage and survival time, making miR-381 a novel prognostic factor.

scholarly journals Curcumin Affects HSP60 Folding Activity and Levels in Neuroblastoma Cells

2020 ◽  
Vol 21 (2) ◽  
pp. 661 ◽  
Author(s):  
Celeste Caruso Bavisotto ◽  
Antonella Marino Gammazza ◽  
Filippa Lo Cascio ◽  
Emanuele Mocciaro ◽  
Alessandra Maria Vitale ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Culture Media ◽  
Neuroblastoma Cell ◽  
Cancer Development ◽  
Protective Mechanism ◽  
Protein Homeostasis ◽  
Matrix Remodeling ◽  
Dependent Manner ◽  
Mesenchymal Transition

The fundamental challenge in fighting cancer is the development of protective agents able to interfere with the classical pathways of malignant transformation, such as extracellular matrix remodeling, epithelial–mesenchymal transition and, alteration of protein homeostasis. In the tumors of the brain, proteotoxic stress represents one of the main triggering agents for cell transformation. Curcumin is a natural compound with anti-inflammatory and anti-cancer properties with promising potential for the development of therapeutic drugs for the treatment of cancer as well as neurodegenerative diseases. Among the mediators of cancer development, HSP60 is a key factor for the maintenance of protein homeostasis and cell survival. High HSP60 levels were correlated, in particular, with cancer development and progression, and for this reason, we investigated the ability of curcumin to affect HSP60 expression, localization, and post-translational modifications using a neuroblastoma cell line. We have also looked at the ability of curcumin to interfere with the HSP60/HSP10 folding machinery. The cells were treated with 6, 12.5, and 25 µM of curcumin for 24 h, and the flow cytometry analysis showed that the compound induced apoptosis in a dose-dependent manner with a higher percentage of apoptotic cells at 25 µM. This dose of curcumin-induced a decrease in HSP60 protein levels and an upregulation of HSP60 mRNA expression. Moreover, 25 µM of curcumin reduced HSP60 ubiquitination and nitration, and the chaperonin levels were higher in the culture media compared with the untreated cells. Furthermore, curcumin at the same dose was able to favor HSP60 folding activity. The reduction of HSP60 levels, together with the increase in its folding activity and the secretion in the media led to the supposition that curcumin might interfere with cancer progression with a protective mechanism involving the chaperonin.

scholarly journals Role of extracellular matrix in breast cancer development: a brief update

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 274 ◽  
Author(s):  
Manoj Kumar Jena ◽  
Jagadeesh Janjanam
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Development ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Breast Cancer Development ◽  
Cancer Pathogenesis

Evidence is increasing on the crucial role of the extracellular matrix (ECM) in breast cancer progression, invasion and metastasis with almost all mortality cases owing to metastasis. The epithelial-mesenchymal transition is the first signal of metastasis involving different transcription factors such as Snail, TWIST, and ZEB1. ECM remodeling is a major event promoting cancer invasion and metastasis; where matrix metalloproteinases (MMPs) such as MMP-2, -9, -11, and -14 play vital roles degrading the matrix proteins for cancer spread. The β-D mannuronic acid (MMP inhibitor) has anti-metastatic properties through inhibition of MMP-2, and -9 and could be a potential therapeutic agent. Besides the MMPs, the enzymes such as LOXL2, LOXL4, procollagen lysyl hydroxylase-2, and heparanase also regulate breast cancer progression. The important ECM proteins like integrins (b1-, b5-, and b6- integrins), ECM1 protein, and Hic-5 protein are also actively involved in breast cancer development. The stromal cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and adipocytes also contribute in tumor development through different processes. The TAMs become proangiogenic through secretion of VEGF-A and building vessel network for nourishment and invasion of the tumor mass. The latest developments of ECM involvement in breast cancer progression has been discussed in this review and this study will help researchers in designing future work on breast cancer pathogenesis and developing therapy targeted to the ECM components.

scholarly journals YAP-Dependent BiP Induction Is Involved in Nicotine-Mediated Oral Cancer Malignancy

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2080
Author(s):  
Chu-Yen Chien ◽  
Ying-Chen Chen ◽  
Chia-Chen Hsu ◽  
Yu-Ting Chou ◽  
Shine-Gwo Shiah ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Er Stress ◽  
Cancer Progression ◽  
Nuclear Translocation ◽  
Epithelial Mesenchymal Transition ◽  
Therapeutic Potential ◽  
Significant Risk ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Α7 Nachr

Cigarette smoking is a significant risk factor for the development and progression of oral cancer. Previous studies have reported an association between nicotine and malignancy in oral cancer. Recent studies have also demonstrated that nicotine can induce endoplasmic reticulum (ER) stress in tumor cells. Binding immunoglobulin protein (BiP) acts as a master regulator of ER stress and is frequently overexpressed in oral cancer cell lines and tissues. However, the effect of nicotine on BiP in oral cancer is unknown. Therefore, this study aimed to evaluate the role of BiP and its underlying regulatory mechanisms in nicotine-induced oral cancer progression. Our results showed that nicotine significantly induced the expression of BiP in time- and dose-dependent manners in oral squamous cell carcinoma (OSCC) cells. In addition, BiP was involved in nicotine-mediated OSCC malignancy, and depletion of BiP expression remarkably suppressed nicotine-induced malignant behaviors, including epithelial–mesenchymal transition (EMT) change, migration, and invasion. In vivo, BiP silencing abrogated nicotine-induced tumor growth and EMT switch in nude mice. Moreover, nicotine stimulated BiP expression through the activation of the YAP-TEAD transcriptional complex. Mechanistically, we observed that nicotine regulated YAP nuclear translocation and its interaction with TEAD through α7-nAChR-Akt signaling, subsequently resulting in increased TEAD occupancy on the HSPA5 promoter and elevated promoter activity. These observations suggest that BiP is involved in nicotine-induced oral cancer malignancy and may have therapeutic potential in tobacco-related oral cancer.

scholarly journals Upregulation of LGALS1 is associated with oral cancer metastasis

2018 ◽  
Vol 10 ◽  
pp. 175883591879462 ◽  
Author(s):  
Ji-Min Li ◽  
Chien-Wei Tseng ◽  
Chi-Chen Lin ◽  
Ching-Hsuan Law ◽  
Yu-An Chien ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Mapk Pathway ◽  
Cancer Tissue ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Background: Oral cancer metastasis is a devastating process that contributes to poor prognosis and high mortality, yet its detailed underlying mechanisms remain unclear. Here, we aimed to evaluate metastasis-specific markers in oral cancer and to provide comprehensive recognition concerning functional roles of the specific target in oral cancer metastasis. Methods: Lectin, galactoside-binding, soluble, 1 (LGALS1) was identified by secretomic analysis. LGALS1 expression of patient samples with oral cancer on the tissue microarray were examined by immunochemical (IHC) staining. Small interfering RNA (siRNA)-mediated knockdown of LGALS1 revealed the role of LGALS1 in oral cancer metastasis in vitro and in vivo. Results: LGALS1 was observed to be upregulated in highly invasive oral cancer cells, and elevated LGALS1 expression was correlated with cancer progression and lymph node metastasis in oral cancer tissue specimens. Functionally, silencing LGALS1 resulted in suppressed cell growth, wound healing, cell migration, and cell invasion in oral cancer cells in vitro. Knockdown of LGALS1 in highly invasive oral cancer cells dramatically inhibited lung metastasis in an in vivo mouse model. Mechanistic studies suggested p38 mitogen-activated protein kinase (MAPK) phosphorylation, upregulated MMP-9, and mesenchymal phenotypes of epithelial-mesenchymal transition (EMT) in highly invasive oral cancer cells, whereas siRNA against LGALS1 resulted in the inactivation of p38 MAPK pathway, downregulated MMP-9, and EMT inhibition. Conclusions: These findings demonstrate that elevated LGALS1 is strongly correlated with oral cancer progression and metastasis, and that it could potentially serve as a prognostic biomarker and an innovative target for oral cancer therapy.

scholarly journals A szájüreg leggyakoribb bakteriális eredetű kórképeinek jellegzetességei, diagnosztikája és kezelése

2019 ◽  
Vol 160 (19) ◽  
pp. 739-746
Author(s):  
Károly Mensch ◽  
Gábor Nagy† ◽  
Ádám Nagy ◽  
Andrea Bródy
Keyword(s):  
Oral Cancer ◽  
Oral Cavity ◽  
Oral Hygiene ◽  
Periodontal Diseases ◽  
Bacterial Species ◽  
Clinical Aspects ◽  
Bacterial Diseases ◽  
Dental Biofilm ◽  
Untreated Caries ◽  
Dental Foci

Abstract: Billions of microorganisms can be found in the oral cavity, from which bacteria are the most frequent. More than 600 bacterial species can be isolated. Most of them are harmless, moreover, some species prove themselves to be specifically useful. However, in the case of a weakened immune status or inappropriate oral hygiene, they may cause many types of soft and hard tissue disorders. Caries and periodontal diseases are the most common bacterial diseases of the oral cavity. In both cases, the dental biofilm gives rise to the disorder, which is caused by the insufficient oral hygiene. Dental caries are mainly caused by cariogenic streptococci and lactobacilli. In the case of serious periodontal diseases, anaerob parodonto-pathogen microorganisms play the major role. Untreated caries may result in the necrosis of the pulp, which can cause an inflammation expanding towards the parodontium. This can be characterized as a focal infection, like the untreated periodontal pockets. Dental foci may have lots of systemic consequences such as cardiovascular diseases, diabetes, pneumonia, arthritis, preterm birth and alopecia areata. When these diseases occur, dental foci should always be considered. The professional plaque control and chlorhexidine rinsing before the proposed surgeries have an outstanding role in the prevention of ventilator-associated pneumonia. Oral cancer is multicausal; more and more researchers are analyzing the role of certain bacteria in the carcinogenesis of oral cancer. In addition to the mentioned clinical aspects, we are planning to describe the relatively rare, but diverse and diagnostically challenging bacterial soft tissue disorders in another publication. Orv Hetil. 2019; 160(19): 739–746.

scholarly journals Does epithelial mesenchymal transition markers snail and slug correlate with clinical stage of oral cancer: a clinico-pathological study of 258 patients

2020 ◽  
Vol 6 (6) ◽  
pp. 1132
Author(s):  
Suvercha Arya ◽  
Vipin Arora ◽  
Harish C. Taneja ◽  
Priyanka Gogoi
Keyword(s):  
Oral Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Clinical Stage ◽  
Clinical Staging ◽  
Head Neck Cancer ◽  
Mesenchymal Transition ◽  
Stage 4 ◽  
Slug Expression ◽  
Stage 1 ◽  
Time Of Presentation

<p class="abstract"><strong>Background:</strong> Head and neck cancers are the 6th most common cancers worldwide. In contrast, according to population-based cancer registries these constitute the commonest cancer in Indian men and third most common cancer in women. Oral cancer is the commonest head neck cancer, attributed to rampant smoking and chewing of tobacco and areca nut in India. Epithelial mesenchymal transition (EMT) is the process in which committed epithelial cells undergo transformation into mesenchymal phenotype, that has invasive properties and thus contribute to metastatic potential of cancers.</p><p class="abstract"><strong>Methods:</strong> The current study was undertaken to correlate the expression of EMT markers snail and slug with tumor stage at the time of presentation.  </p><p class="abstract"><strong>Results:</strong> In present study, snail positivity was 60% in patients presenting at stage 1, 73% in stage 2, 85% in stage 3 and 90% in stage 4 patients. There was no significant association between clinical staging and snail positivity (p=0.549). Slug positivity was 40% in patients presenting at stage 1, 26.7% in stage 2, 59% in stage 3 and 77% in stage 4 patients. There was significant association between clinical staging and Slug positivity (p=0.002). Either snail or slug expression was found in 89.53% patients.</p><p class="abstract"><strong>Conclusions:</strong> We found that EMT marker slug expression was significantly associated with advanced clinical stage of oral cancer at the time of presentation.</p><p class="abstract"> </p>

scholarly journals Role of extracellular matrix in breast cancer development: a brief update

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 274 ◽  
Author(s):  
Manoj Kumar Jena ◽  
Jagadeesh Janjanam
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Development ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Breast Cancer Development ◽  
Cancer Pathogenesis

Evidence is increasing on the crucial role of the extracellular matrix (ECM) in breast cancer progression, invasion and metastasis with almost all mortality cases owing to metastasis. The epithelial-mesenchymal transition is the first signal of metastasis involving different transcription factors such as Snail, TWIST, and ZEB1. ECM remodeling is a major event promoting cancer invasion and metastasis; where matrix metalloproteinases (MMPs) such as MMP-2, -9, -11, and -14 play vital roles degrading the matrix proteins for cancer spread. The β-D mannuronic acid (MMP inhibitor) has anti-metastatic properties through inhibition of MMP-2, and -9 and could be a potential therapeutic agent. Besides the MMPs, the enzymes such as LOXL2, LOXL4, procollagen lysyl hydroxylase-2, and heparanase also regulate breast cancer progression. The important ECM proteins like integrins (b1-, b5-, and b6- integrins), ECM1 protein, and Hic-5 protein are also actively involved in breast cancer development. The stromal cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and adipocytes also contribute in tumor development through different processes. The TAMs become proangiogenic through secretion of VEGF-A and building vessel network for nourishment and invasion of the tumor mass. The latest developments of ECM involvement in breast cancer progression has been discussed in this review and this study will help researchers in designing future work on breast cancer pathogenesis and developing therapy targeted to the ECM components.

scholarly journals Is There an Interconnection between Epithelial–Mesenchymal Transition (EMT) and Telomere Shortening in Aging?

2021 ◽  
Vol 22 (8) ◽  
pp. 3888
Author(s):  
Siti A. M. Imran ◽  
Muhammad Dain Yazid ◽  
Ruszymah Bt Hj Idrus ◽  
Manira Maarof ◽  
Abid Nordin ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Cell Biology ◽  
Epithelial Mesenchymal Transition ◽  
Primitive Streak ◽  
Vital Role ◽  
Potential Interaction ◽  
Cancer Development ◽  
Mesenchymal Transition ◽  
Age Related ◽  
Type 3

Epithelial–Mesenchymal Transition (EMT) was first discovered during the transition of cells from the primitive streak during embryogenesis in chicks. It was later discovered that EMT holds greater potential in areas other than the early development of cells and tissues since it also plays a vital role in wound healing and cancer development. EMT can be classified into three types based on physiological functions. EMT type 3, which involves neoplastic development and metastasis, has been the most thoroughly explored. As EMT is often found in cancer stem cells, most research has focused on its association with other factors involving cancer progression, including telomeres. However, as telomeres are also mainly involved in aging, any possible interaction between the two would be worth noting, especially as telomere dysfunction also contributes to cancer and other age-related diseases. Ascertaining the balance between degeneration and cancer development is crucial in cell biology, in which telomeres function as a key regulator between the two extremes. The essential roles that EMT and telomere protection have in aging reveal a potential mutual interaction that has not yet been explored, and which could be used in disease therapy. In this review, the known functions of EMT and telomeres in aging are discussed and their potential interaction in age-related diseases is highlighted.

scholarly journals Human Papillomavirus 16 E7 Promotes EGFR/PI3K/AKT1/NRF2 Signaling Pathway Contributing to PIR/NF-κB Activation in Oral Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1904 ◽  
Author(s):  
Diego Carrillo-Beltrán ◽  
Juan P. Muñoz ◽  
Nahir Guerrero-Vásquez ◽  
Rancés Blanco ◽  
Oscar León ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Oral Cancer ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Hpv Infection ◽  
Mesenchymal Transition ◽  
Human Papillomavirus 16 ◽  
Nrf2 Signaling Pathway ◽  
E6 And E7 ◽  
Oral Cancer Cells

A subset of oral carcinomas is etiologically related to high-risk human papillomavirus (HR-HPV) infection, with HPV16 being the most frequent HR-HPV type found in these carcinomas. The oncogenic role of HR-HPV is strongly dependent on the overexpression of E6 and E7 oncoproteins, which, in turn, induce p53 and pRb degradation, respectively. Additionally, it has been suggested that HR-HPV oncoproteins are involved in the regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), inducing cancer progression and metastasis. Previously, we reported that HPV16 E7 oncoprotein promotes Pirin upregulation resulting in increased epithelial–mesenchymal transition (EMT) and cell migration, with Pirin being an oxidative stress sensor and activator of NF-κB. In this study, we demonstrate the mechanism by which HPV16 E7-mediated Pirin overexpression occurs by promoting EGFR/PI3K/AKT1/NRF2 signaling, thus causing PIR/NF-κB activation in oral tumor cells. Our results demonstrate a new mechanism by which E7 contributes to oral cancer progression, proposing PIR as a potential new therapeutic target.

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