Huixu Xie1, Chuansong Li2, Yan He3, Robert Griffin3, Qingsong Ye4, Longjiang Li5. 1. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China; West China School of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China; College of Medicine and Dentistry, James Cook University, Cairns, QLD 4878, Australia. 2. Medical Scientific Academy in Sichuan People's Hospital, Chengdu, Sichuan 610031, China. 3. College of Medicine and Dentistry, James Cook University, Cairns, QLD 4878, Australia. 4. College of Medicine and Dentistry, James Cook University, Cairns, QLD 4878, Australia. Electronic address: qingsongye@hotmail.com. 5. State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China; West China School of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China. Electronic address: muzili63@163.com.
Abstract
OBJECTIVES: Chronic stress was previously reported to play a role in the development of oral cancer, yet the correlation between stressors and oral cancer progression is not well understood. MATERIALS AND METHODS: We implanted human oral cancer cell line CAL 27 in nude mice to investigate the effects of chronic stress on tumor growth, and designed a physical restraint system to create an experimentally stressed animal model, in which periodic immobilization induced characteristic chronic stress. Tumor burdened animal were randomly assigned into four groups: (a) control group, (b) daily stress for 2h with light, (c) daily stress for 2h in dark, and (d) daily stress for 6h with light. Animals were sacrificed after three weeks. Various analyses were performed on parameters including body weight, tumor weight, in situ expression of MMP-2 and VEGF, and the plasma concentrations of epinephrine, norepinephrine and glucocorticoid. RESULTS AND CONCLUSION: Our data showed that chronic stress resulted in greater tumor size, more expression of MMP-2 and VEGF, higher level of plasma catecholamines, and more invasive growth of oral carcinoma cells in a mice model. We have successfully set up an animal model, which studied the effect of chronic stress on oral carcinoma growth rate and progression. These data further suggested that catecholamine and glucocorticoid might stimulate tumor progression under chronic stress.
OBJECTIVES: Chronic stress was previously reported to play a role in the development of oral cancer, yet the correlation between stressors and oral cancer progression is not well understood. MATERIALS AND METHODS: We implanted humanoral cancer cell line CAL 27 in nude mice to investigate the effects of chronic stress on tumor growth, and designed a physical restraint system to create an experimentally stressed animal model, in which periodic immobilization induced characteristic chronic stress. Tumor burdened animal were randomly assigned into four groups: (a) control group, (b) daily stress for 2h with light, (c) daily stress for 2h in dark, and (d) daily stress for 6h with light. Animals were sacrificed after three weeks. Various analyses were performed on parameters including body weight, tumor weight, in situ expression of MMP-2 and VEGF, and the plasma concentrations of epinephrine, norepinephrine and glucocorticoid. RESULTS AND CONCLUSION: Our data showed that chronic stress resulted in greater tumor size, more expression of MMP-2 and VEGF, higher level of plasma catecholamines, and more invasive growth of oral carcinoma cells in a mice model. We have successfully set up an animal model, which studied the effect of chronic stress on oral carcinoma growth rate and progression. These data further suggested that catecholamine and glucocorticoid might stimulate tumor progression under chronic stress.
Authors: Divya Nedungadi; Nathan Ryan; Kelvin Anderson; Felipe F Lamenza; Pete P Jordanides; Michael J Swingler; Liva Rakotondraibe; Kenneth M Riedl; Hans Iwenofu; Steve Oghumu Journal: Carcinogenesis Date: 2022-02-11 Impact factor: 4.944
Authors: Daniela B Bastos; Bruna A M Sarafim-Silva; Maria Lúcia M M Sundefeld; Amanda A Ribeiro; Juliana D P Brandão; Éder R Biasoli; Glauco I Miyahara; Dulce E Casarini; Daniel G Bernabé Journal: PLoS One Date: 2018-08-20 Impact factor: 3.240