Obesity can Inhibit a Key Cancer Defense Mechanism
Sasaki A, Nagatake T, Egami R, Gu G, Takigawa I, Ikeda W, Nakatani T, Kunisawa J, Fujita Y. Obesity Suppresses Cell-Competition-Mediated Apical Elimination of RasV12-Transformed Cells from Epithelial Tissues. Cell Reports, 2018; 23 (4): 974 DOI: 10.1016/j.celrep.2018.03.104
Obesity can Inhibit a Key Cancer Defense Mechanism
A recent Japanese study has linked high body fat to a suppression of a specific cancer defense mechanism and higher rates of tumor formation in fatter lab mice. The affected cellular mechanism is known as cellular competition, when cells compete with other surrounding cells for survival, killing transformed cells that could be malignant. The surrounding cells use their cytoskeletal protein filamin to suppress the growth of altered cells and stop further cancer growth. Normal epithelial cells have anti-tumor actions that do not involve immune cells, this mechanism is called epithelial defense against cancer (EDAC) (Sasaki et al.)
Genetically modified mice were used in this study to express the more RasV12 cells (cells that are suppressed by the EDAC mechanism). They were also marked with cytokeratin 19 in order to follow the cytoskeletal movements in the EDAC mechanism. For three months some mice were fed a normal diet while others were fed a high fat diet, which induced obesity.
Obese mice showed a significantly suppressed frequency of apical extrusion of RasV12 cells in the small intestine and pancreas, but not in lung tissue, indicating obesity can suppress elimination of transformed cells in certain tissues, but not all. Tamoxifen was injected into the mice to induce the RasV12 cell expression. Obese mice began to form pancreatic tumors from the RasV12 cells that had not been eliminated by EDAC mechanisms.
The findings of this study indicate that obesity can increase the risk of tumor formation in intestinal and pancreatic cells, but not lung cells. Reducing obesity will reduce chronic inflammation of the body's epithelial cells and allow for proper mechanisms to prevent cancer and metabolic diseases.
-CK
Obesity can Inhibit a Key Cancer Defense Mechanism
A recent Japanese study has linked high body fat to a suppression of a specific cancer defense mechanism and higher rates of tumor formation in fatter lab mice. The affected cellular mechanism is known as cellular competition, when cells compete with other surrounding cells for survival, killing transformed cells that could be malignant. The surrounding cells use their cytoskeletal protein filamin to suppress the growth of altered cells and stop further cancer growth. Normal epithelial cells have anti-tumor actions that do not involve immune cells, this mechanism is called epithelial defense against cancer (EDAC) (Sasaki et al.)
Genetically modified mice were used in this study to express the more RasV12 cells (cells that are suppressed by the EDAC mechanism). They were also marked with cytokeratin 19 in order to follow the cytoskeletal movements in the EDAC mechanism. For three months some mice were fed a normal diet while others were fed a high fat diet, which induced obesity.
Obese mice showed a significantly suppressed frequency of apical extrusion of RasV12 cells in the small intestine and pancreas, but not in lung tissue, indicating obesity can suppress elimination of transformed cells in certain tissues, but not all. Tamoxifen was injected into the mice to induce the RasV12 cell expression. Obese mice began to form pancreatic tumors from the RasV12 cells that had not been eliminated by EDAC mechanisms.
The findings of this study indicate that obesity can increase the risk of tumor formation in intestinal and pancreatic cells, but not lung cells. Reducing obesity will reduce chronic inflammation of the body's epithelial cells and allow for proper mechanisms to prevent cancer and metabolic diseases.
-CK
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