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Subvert cognition! Nanjing University found that high salt diet can inhibit tumor growth

Hits: 3893212 2020-04-13

By nagashi
Eating habits have a significant impact on people's health. Different families have different eating habits, and even different regions will form different eating styles. However, some eating habits, such as high salt diet, are generally accepted and have a negative impact on health.
Excessive salt intake (NaCl) is clearly defined as an unhealthy lifestyle because of its strong correlation with the high risk of chronic inflammation, cardiovascular disease and autoimmune diseases. Therefore, many experts and scholars suggest that the upper limit of daily salt intake is 3.75-6g. From this point of view, high salt diet seems to be harmful without any benefit. However, a new study shows that high salt diet can inhibit tumor growth! Recently, researchers from the State Key Laboratory of pharmaceutical biotechnology, School of life sciences, Nanjing University published a research paper on nature communications entitled: high salt die in hibits tumour growth in mice via regulating myoid derived regulator cell differentiation. This study shows that high salt diet can activate anti-tumor immune monitoring by regulating the activity of bone marrow-derived inhibitory cells (MDSCs), so as to inhibit the growth of tumor in mice. More and more evidences show that high salt diet can lead to the disorder of immune system, promote immune cells to secrete more cytokines, and then induce inflammation in various tissue microenvironment. However, in tumor microenvironment, the key to overcome immunosuppression and recover the immune attack to tumor is to stimulate the pro-inflammatory activity of various cell types. Bone marrow derived inhibitory cells (MDSCs) play an important role in tumor induced immune tolerance. MDSCs are immature myeloid cells, which are divided into monocyte MDSCs (m-mdscs) and granulocyte MDSCs (PMN MDSCs). Hypertonic osmolality caused by high salt intake is a typical environmental stimulus that can be felt by cells, and can cause the immune response of macrophages mediated by transcription factor (NFAT5). It has been shown that p38 / NFAT5 pathway can enhance the expression of many pro-inflammatory genes and promote the survival of macrophages. In this study, the researchers hypothesized that high salt diet can stimulate MDSCs in tumor microenvironment to form immune stimulating phenotype, thus inhibiting tumor progression. In this regard, the researchers constructed two kinds of allogeneic tumor mice models and fed them with high salt food to observe the effect of high salt diet on tumor growth. The researchers found that a high salt diet increased the local concentration of NaCl in tumor tissue, leading to hypertonic osmolality, and reduced the production of cytokines required for MDSCs amplification and their aggregation in blood, spleen and tumor. Therefore, two cell subsets of MDSCs change their phenotypes. M-mdscs differentiate into anti-tumor macrophages. PMN MDSCs have the effect of promoting inflammation, thus reactivating the anti-tumor effect of T cells. In addition, the researchers also found that high salt diet enhanced the anti-tumor activity of PD-1 inhibitors, and enhanced the expression of proinflammatory factors and anti-tumor immune response by regulating p38 / mapk-nfat5 signal pathway. All in all, this study found that high salt diet can activate anti-tumor immune response by regulating the activity of bone marrow-derived inhibitory cells (MDSCs), so as to inhibit the growth of tumor. The findings overturn previous perceptions that a high salt diet is not always harmful, at least for cancer treatment. Special reminder: high salt diet more or through the regulation of the body's immune system to inhibit tumor growth, but in the final analysis, excessive salt intake is still an unhealthy way of life, trying to cure tumors through high salt diet is undoubtedly "drinking poison to quench thirst", the scientific significance of this study is more than practical value. Paper link: https://doi.org/10.1038/s41467-020-15524-1
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