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Is Peripheral Benzodiazepine Receptor (PBR) Gene Expression Involved in Breast Cancer Suppression by Dietary Soybean Protein

机译:外周苯二氮卓受体(pBR)基因表达参与饮食大豆蛋白抑制乳腺癌

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Among many environmental factors, dietary factors play an important role in the development and progression of breast cancer. It has been established that women in Asian countries consume more soy protein than women in the United States and that the incidence of breast cancer in women in Asian countries is generally lower. While this association is correlative and no causative effect has been demonstrated, an increasing body of evidence suggests that soy protein consumption may be protective, thus reducing the risk of breast cancer development. The purpose of this study was to elucidate the molecular mechanism(s) by which dietary soy protein may offer its tumor suppressing effect. We developed a breast cancer model in female rats in which soy protein replaced case in as the dietary source of protein to investigate whether tumor development can be counteracted. The results showed a delay in the tumor formation and also a protection against the aggressiveness of the tumors in the soy protein group than in the casein group. The aggressive phenotype expression of breast cancer was correlated with the increased expression of a particular gene, peripheral benzodiazepine receptors (PBRs), implicating PBRs to be considered as a cancer promoting gene. Furthermore, the aggressive phenotype expression of breast cancer, such as increased ligand binding, increased gene expression and possible mutation(s), PBRs-mediated cholesterol transport into the nucleus, and NTPase activity of breast epithelial cells was controlled by dietary consumption of soy protein. Our studies also revealed that PBRs may play an important role in angiogenesis, and expression of some key angiogenic factors, such as b-FGF and VEGF in breast tumors was lower in soy protein group than in case in group. Therefore, it can be suggested that the breast cancer suppressing effect of dietary soy protein is mediated by inhibition of PBRs-mediated angiogenic signaling.

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