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Social isolation stress facilitates chemically induced oral carcinogenesis
PLOS ONE ( IF 2.9 ) Pub Date : 2021-01-07 , DOI: 10.1371/journal.pone.0245190
Flávia Alves Verza 1 , Vitor Bonetti Valente 1 , Lia Kobayashi Oliveira 1 , Giseli Mitsuy Kayahara 1, 2 , Marcelo Macedo Crivelini 2 , Cristiane Furuse 2 , Éder Ricardo Biasoli 1, 2 , Glauco Issamu Miyahara 1, 2 , Sandra Helena Penha Oliveira 3 , Daniel Galera Bernabé 1, 2
Affiliation  

Social isolation has affected a large number of people and may lead to impairment of physical and mental health. Although stress resulting from social isolation may increase cancer progression, its interference on tumorigenesis is poorly known. In this study, we used a preclinical model to evaluate the effects of social isolation stress on chemically induced oral carcinogenesis. Sixty-two 21-day-old male Wistar rats were divided into isolated and grouped groups. After 90 days of age, the rats from both groups underwent oral carcinogenesis with 4-nitroquinoline 1-oxide (4NQO) for 20 weeks. All rats were assessed for depressive-like behavior and euthanized for oral squamous cell carcinoma (OSCC) diagnosis and measurement of inflammatory mediators in the tumor microenvironment. Social isolation stress increased the OSCC occurrence by 20.4% when compared to control. Isolated rats also showed higher tumor volume and cachexia than the grouped rats. Social isolation did not induce changes in the depressive-like behavior after carcinogenic induction. Tumors from stressed rats had increased levels of the inflammatory mediators, TNF-alpha, IL1-beta and MCP-1. The concentrations of TNF-alpha and MCP-1 were significantly increased in the large tumors from isolated animals. Higher tumor levels of TNF-alpha, IL-6, IL1-beta and MCP-1 were positively correlated with OSCC growth. This study provides the first evidence that social isolation stress may facilitate OSCC occurrence and tumor progression, an event accompanied by increased local levels of inflammatory mediators.



中文翻译:

社会隔离压力促进化学诱导的口腔癌发生

社会孤立影响了很多人,并可能导致身心健康受损。尽管社会隔离造成的压力可能会增加癌症的进展,但其对肿瘤发生的干扰却鲜为人知。在这项研究中,我们使用临床前模型来评估社会隔离压力对化学诱导的口腔癌发生的影响。将 62 只 21 天大的雄性 Wistar 大鼠分成隔离组和分组。90 天后,两组大鼠都接受了 4-硝基喹啉 1-氧化物 (4NQO) 为期 20 周的口腔致癌作用。评估所有大鼠的抑郁样行为,并实施安乐死以进行口腔鳞状细胞癌 (OSCC) 诊断和肿瘤微环境中炎症介质的测量。社会孤立压力使 OSCC 的发生率增加了 20。与对照相比为 4%。与分组的大鼠相比,孤立的大鼠也显示出更高的肿瘤体积和恶病质。致癌诱导后,社会隔离不会引起抑郁样行为的变化。来自应激大鼠的肿瘤增加了炎症介质、TNF-α、IL1-β 和 MCP-1 的水平。离体动物的大肿瘤中 TNF-α 和 MCP-1 的浓度显着增加。肿瘤坏死因子-α、IL-6、IL1-β 和 MCP-1 的较高肿瘤水平与 OSCC 生长呈正相关。这项研究提供了第一个证据,表明社会隔离压力可能促进 OSCC 的发生和肿瘤进展,这一事件伴随着局部炎症介质水平的增加。致癌诱导后,社会隔离不会引起抑郁样行为的变化。来自应激大鼠的肿瘤增加了炎症介质、TNF-α、IL1-β 和 MCP-1 的水平。离体动物的大肿瘤中 TNF-α 和 MCP-1 的浓度显着增加。肿瘤坏死因子-α、IL-6、IL1-β 和 MCP-1 的较高肿瘤水平与 OSCC 生长呈正相关。这项研究提供了第一个证据,表明社会隔离压力可能促进 OSCC 的发生和肿瘤进展,这一事件伴随着局部炎症介质水平的增加。致癌诱导后,社会隔离不会引起抑郁样行为的变化。来自应激大鼠的肿瘤增加了炎症介质、TNF-α、IL1-β 和 MCP-1 的水平。离体动物的大肿瘤中 TNF-α 和 MCP-1 的浓度显着增加。肿瘤坏死因子-α、IL-6、IL1-β 和 MCP-1 的较高肿瘤水平与 OSCC 生长呈正相关。这项研究提供了第一个证据,表明社会隔离压力可能促进 OSCC 的发生和肿瘤进展,这一事件伴随着局部炎症介质水平的增加。离体动物的大肿瘤中 TNF-α 和 MCP-1 的浓度显着增加。肿瘤坏死因子-α、IL-6、IL1-β 和 MCP-1 的较高肿瘤水平与 OSCC 生长呈正相关。这项研究提供了第一个证据,表明社会隔离压力可能促进 OSCC 的发生和肿瘤进展,这一事件伴随着局部炎症介质水平的增加。离体动物的大肿瘤中 TNF-α 和 MCP-1 的浓度显着增加。肿瘤坏死因子-α、IL-6、IL1-β 和 MCP-1 的较高肿瘤水平与 OSCC 生长呈正相关。这项研究提供了第一个证据,表明社会隔离压力可能促进 OSCC 的发生和肿瘤进展,这一事件伴随着局部炎症介质水平的增加。

更新日期:2021-01-07
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