Current mouse models of oral squamous cell carcinoma: Genetic and chemically induced models

Ishida, Kazuhisa; Tomita, Hiroyuki; Nakashima, Toshihiko; Hirata, Akihiro; Tanaka, T; Shibata, Toshiyuki; Hara, Akira

doi:10.1016/j.oraloncology.2017.07.028

Cited by 78 publications

(91 citation statements)

References 46 publications

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“…8 Employing in vivo animal models as research subjects renders the initiation, promotion, development and metastasis of cancer, including oral cancer, observable. 9 Therefore, this study was conducted using 3-month-old, male, Wistar rats (Rattus norvegicus) which represent the most widely employed animal subjects for laboratory research and which, at the age of three months, have reached biological maturity. 10 Male Wistar rats were chosen as research subjects because their conditions are not affected by hormonal factors, such as the menstrual cycle and pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa

et al. 2019

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Background: Smoking, both active and passive, has been widely recognised as toxic to the human body, since it induces several forms of cancer, including that affecting the oral cavity. Benzopyrene, the carcinogen contained in tobacco smoke, can even lead tocarcinogenesis which potentially affects the regulation of cell apoptosis in both active and passive smokers. Purpose: This study aims to investigate the carcinogenic effects of cigarette smoke on apoptosis of rat tongue mucosae through p53 expression. To determine the risk of malignant transformation through tumor suppressor genes in the apoptotic pathway. Methods: Rattus norvegicus subjects were divided into four groups, namely Treatment Group 1 exposed to sidestream cigarette smoke for four weeks (P1), Treatment Group 2 exposed to sidestream cigarette smoke for eight weeks (P2), Control Group not exposed to sidestream cigarette smoke for four weeks (K2), and Control Group (K) not exposed to sidestream cigarette smoke for eight weeks (K2). The exposure process was conducted using a smoking pump and alternating exposure. Four micron-thick sections of formalin were subsequently fixed together with paraffin embedded biopsy material from tongue mucosa of Rattus norvegicus. The tissue sections from the treatment groups were then analyzed immunohistochemically to compare the expressions of p53 and Bcl-2 proteins with those of the control groups. Results: The T-test results indicated statistically significant differences in the expressions of p53 between the 4-week control group (K1) and the 4-week treatment group (P1) (p=0.01, p<0.05) as well as between the 8-week control group (K2) and the 8-week treatment group (P2) (p=0.03, p<0.05). Conclusion: Exposure to cigarette smoke can induce changes in tumor suppressor genes and also affect the regulation of cell apoptosis, thus changing cell structure and leading to malignancy.

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Section: Discussionmentioning

confidence: 99%

Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa

et al. 2019

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“…The spatial specificity or tissue specificity in conditional GEMMs is determined by Cre transgenes that are expressed from tissuespecific promoters (29). For the oral cavity, the known optimal promoters are the keratin 5 (K5) and keratin 14 (K14) promoters (177). K5 is expressed within the basal layer of the tongue and forestomach stratified squamous epithelia, while K14 has been found to be expressed in the basal layer of the oral mucosa and tongue (185).…”

Section: Methods Of Gemmsmentioning

confidence: 99%

“…Genetically modified mouse models, also known as genetically engineered mouse models (GEMMs), are intricate and novel animal models that have been a beneficial outcome of the development of genetic engineering technology. A review of GEMMs of OSCC was published by Ishida et al (177), so we mainly provide an overview of GEMMs.…”

Section: Genetically Modified Mouse Modelsmentioning

confidence: 99%

Mouse Tumor-Bearing Models as Preclinical Study Platforms for Oral Squamous Cell Carcinoma

Dong

Yang

et al. 2020

Front. Oncol.

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Preclinical animal models of oral squamous cell carcinoma (OSCC) have been extensively studied in recent years. Investigating the pathogenesis and potential therapeutic strategies of OSCC is required to further progress in this field, and a suitable research animal model that reflects the intricacies of cancer biology is crucial. Of the animal models established for the study of cancers, mouse tumor-bearing models are among the most popular and widely deployed for their high fertility, low cost, and molecular and physiological similarity to humans, as well as the ease of rearing experimental mice. Currently, the different methods of establishing OSCC mouse models can be divided into three categories: chemical carcinogen-induced, transplanted and genetically engineered mouse models. Each of these methods has unique advantages and limitations, and the appropriate application of these techniques in OSCC research deserves our attention. Therefore, this review comprehensively investigates and summarizes the tumorigenesis mechanisms, characteristics, establishment methods, and current applications of OSCC mouse models in published papers. The objective of this review is to provide foundations and considerations for choosing suitable model establishment methods to study the relevant pathogenesis, early diagnosis, and clinical treatment of OSCC.

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“…Oral cancer is an increasing threat worldwide, with around 640,000 new cases being detected annually globally. 1,2 In addition, there are 145,000 deaths per year in oral cancer, 3 and five-year survival rates of patients with advanced oral cancer are 30-40%. 4 Owing to the lack of early symptoms and appropriate screening for precancerous lesions, most oral cancer cases are not detected until later stages.…”

Section: Introductionmentioning

confidence: 99%

<p>Genipin Induces Autophagy and Suppresses Cell Growth of Oral Squamous Cell Carcinoma via PI3K/AKT/MTOR Pathway</p>

Wei

Liu

et al. 2020

DDDT

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Background: Oral squamous cell carcinoma (OSCC) is a common malignant tumor of the head and neck, and it accounts for more than 90% of oral cancer. Due to high mortality, limitations of traditional treatment and many complications, new treatment methods are urgently needed. This study aimed to look into the effect of new potential anti-tumor drug, genipin, on OSCC treatment. Methods: In vitro, CCK-8, colony formation, and flow cytometry were used to detect the effect of genipin on SCC-9 and SCC-15 cell lines. Immunofluorescence, real-time PCR, and Western blotting were used to investigate its mechanism. Xenograft tumor model was used to explore the role of genipin in vivo. Results: We found that genipin suppressed cell growth and induced apoptosis in vitro. In addition, the expression of p62 was down-regulated while Beclin1 and LC3II were up-regulated in SCC-25 and SCC-9 cells. 3-methyladenine (3-MA) significantly decreased LC3 (LC3II) + puncta, but genipin rescuect 3d this reduction. Furthermore, genipin also reduced the expression of p-PI3K, p-AKT, and p-mTOR. In vivo experiment showed that genipin significantly curbed the tumor size and weight. The positive expression of Ki67 protein and number of apoptotic cells were increased. Conclusion: Conclusively, this study implicated that genipin suppresses cell proliferation and stimulated apoptosis, and is the first exploration showing that genipin induces OSCC cell autophagy via PI3K/AKT/mTOR pathway inhibition.

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Current mouse models of oral squamous cell carcinoma: Genetic and chemically induced models

Cited by 78 publications

References 46 publications

Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa

Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa

Mouse Tumor-Bearing Models as Preclinical Study Platforms for Oral Squamous Cell Carcinoma

<p>Genipin Induces Autophagy and Suppresses Cell Growth of Oral Squamous Cell Carcinoma via PI3K/AKT/MTOR Pathway</p>

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