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—— Do not pretend to subvert a century of cognition and respect nature.
On April 7, Nature magazine published an online article entitled "Cell-programmed nutrient partitioning in the tumour microenvironment" (the mechanism of cell-programmed nutrient partitioning in the tumour microenvironment) the study.
This study shows the tumor microenvironment (TME) as a whole function of hyperglycemic aerobic glycolysis, and further shows that the tumor microenvironment with hyperaerobic glycolysis plays an important role in the immune escape and progression of tumors.
.
TME, mainly composed of tumor cells, surrounding immune and inflammatory cells, tumor-related fibroblasts, and nearby interstitial tissues, capillaries, and various cytokines and chemokines, is a complex integrated system.
The earliest discovery of sugar phagocytosis in tumor tissues: Warburg effect In the 1920s, the Nobel Prize winner in Physiology and Medicine, German biochemist Otto Heinrieh Warburg, measured the inflow of normal tissue and tumor tissue into arteries and outflow veins in animals Changes in blood sugar have found that even in an environment with adequate oxygen supply, tumor tissues are more inclined to obtain energy through glycolysis.
Application of Glycophagocytosis in Tumor Tissue: FDG-PET In 2009, Professor Vander published a paper in Science, which further confirmed the existence of the Warburg effect and its importance to the growth of tumor cells.
Taking advantage of the high glucose uptake characteristics of tumors, a method (FDG-PET) for tumor diagnosis and treatment effects was developed.
He also believes that dietary supplementation and strict glucose control can help treat tumors.
Tumor tissue sugar phagocytosis research: the heat will not decrease in 2020, and the exploration of the mechanism is beginning to dawn.
In 2020, Science Signaling and Nature Review Cancer have successively published articles to further clarify the mechanism of tumor Warburg effect, and explore the specificity of various gene mutations or autoimmune functions and tumor cells The relationship between sex metabolism helps to better develop tumor treatment methods or enhance the efficacy of drugs.
In November 2020, Sci signal published the research results of Professor Birts' team.
Professor Birts used a human breast cancer cell model to explore the relationship between the tumor suppressor gene p53 and aerobic glycolysis in cancer cells.
P53 is a key gene that regulates metabolic balance and reduces cell damage under metabolic imbalances.
Due to the lack of mature blood supply in tumors and the gradual increase in aerobic glycolysis, lactic acid accumulates, which leads to acidification of TME and inhibits LDH, which leads to tumor cells.
The ratio of internal NADH:NAD+ increases.
This can cause mutations in p53, which regulates glycolysis of tumor cells, promote metabolic imbalance, and further increase the level of aerobic glycolysis of tumor cells, so that tumor cells continue to proliferate in an environment of metabolic imbalance, and high-speed proliferation promotes survival of tumor cells The screening and iteration of the tumor led to the further progress of the tumor.
NADH-CtBP-p53 pathway regulates glycolysis homeostasis model tumor tissue glycophagocytosis 2021 Nature study: Cancer cells in the tumor microenvironment take up 2/3 of glucose, and bone marrow cells take up the other 1/3.
The latest nature study is demonstrated by using PET Tracer to locate and measure specific cell subpopulations in TME to study glucose uptake.
The study further confirmed that the ability of TME to take up glucose is much better than that of normal tissues.
At the same time, it was found that the glucose uptake of individual immune cells in TME was higher than that of tumor cells, but in terms of TME as a whole, tumor cells were still the cell population with the highest sugar addiction.
The researchers multiplied the glucose uptake of each cell by the number of cells of each type, and found that cancer cells (CD45-) accounted for about 2/3 of the total glucose uptake, myeloid immune cells (CD11B+) accounted for the other 1/3, and other immune cells The contribution of cells (CD3+ and other CD45+) is negligible.
Tumors take up more glucose than normal tissue cells.
Cancer cells in tumor tissues take up more glucose as a whole.
(Note: In the text, CD45- cells are mainly cancer cells, CD45+ cells are immune cells, CD11B+ cells are myeloid immune cells, and CD3+ cells are T Cells) In the study, CD45+ flow cytometry was used to isolate CD11B+ labeled myeloid cells.
Compared with other CD45+ cells, myeloid cells (mainly macrophages) have the highest levels of glucose uptake.
Myeloid immune cells (macrophages) in TME can be divided into M1 type and M2 type macrophages.
M1 type macrophages can kill tumor cells and inhibit tumor cell growth through phagocytosis and mediate Th1 response; M2 type macrophages can promote tissue repair, blood vessel formation, and immunity by producing cytokines and mediating Th2 response Inhibition further contributes to the evolution of tumors.
At present, more and more studies have found that the expression of glycolytic transcription genes in tumor cells can induce TME immunosuppression and directly induce immunosuppressive myeloid cell aggregation.
That is, the specific microenvironment of the tumor forces the phenotype of the macrophages entering the tumor to evolve in a direction that is beneficial to the development of the tumor, that is, the production of M2 macrophages.
Based on this, it can be inferred that macrophages that take up a large amount of glucose in TME will promote their continuous transition to M2 type under a large amount of glucose supply and aerobic glycolysis, thereby promoting tumor progression.
TME is a functional whole.
Tumor cells can be regarded as seeds, and other components are regarded as soil.
Tumor cells interact with other components in the environment and evolve together, which promotes the generation of tumors.
High aerobic glycolysis of tumor cells and myeloid cells, a large amount of lactic acid and H+ accumulate in TME, which affects the proliferation, survival, cytotoxicity and cytokine production of infiltrating T cells, destroys the immune balance in TME, and is beneficial to tumor cell immunity Escape and progress.
The role of fat in the tumor microenvironment: A 2020 Nature sub-Journal study suggests that it may promote the conversion of M2 to M1, which is different from focusing on high-sugar supply.
Another recent study focused on the impact of high-fat supply on tumors. In 2020, an animal experiment conducted by Nature’s sub-Journal Signal Transduction and Targeted Therapy showed that a high-fat diet can inhibit the peritoneal dissemination of colorectal cancer (CRC) cells.
The study pointed out that high fat intake can transform macrophages from M2 type to M1-like phenotype, and stimulate TLR4-dependent M1 macrophage activation and phagocytosis in adipose tissue macrophages, further enhancing CD4+ and CD8+ in visceral fat The recruitment (through Cxcl10) and activation (through M1 cytokines) of T cells will ultimately prevent the metastasis and spread of colorectal cancer.
It can be seen that perhaps by increasing the fat-to-energy ratio in the diet, tumor progression can be inhibited and survival rates improved.
High-fat diet promotes the activation of M1 macrophages.
Summary After nearly 100 years of continuous research, scientists have continuously deepened their understanding of tumor metabolism.
Professor Warburg discovered that the uptake of sugar by tumor tissues is more vigorous a hundred years ago.
Today, our research can go deep into the tumor microenvironment and explore the relationship between the metabolism of different cells and the development of tumors.
Finally, I quote Nature, the first sentence of the latest research, to review the essence of the research and development over the past century: "Tumor cells specifically consume glucose through Warburg metabolism, which is the basis of PET tumor imaging.
Tumor infiltrating immune cells also Rely on glucose, and the metabolism of these impaired immune cells in the tumor microenvironment helps tumor cells to achieve immune escape.
" Therefore, we should limit the sugar intake of tumor patients in clinical practice to reduce the impact of sugar metabolism on the development and development of tumors.
. References: 1.
Reinfeld BI, et al.
Cell-programmed nutrient partitioning in the tumour microenvironment.
Nature.
2021 Apr 7.
doi: 10.
1038/s41586-021-03442-1.
Epub ahead of print.
PMID: 33828302.
2.
Warburg O , Wind F, Negelein E.
THE METABOLISM OF TUMORS IN THE BODY.
J Gen Physiol.
1927 Mar 7;8(6):519-30.
doi: 10.
1085/jgp.
8.
6.
519.
PMID: 19872213; PMCID: PMC2140820.
3.
Vander Heiden MG, et al.
Science 2009; 324:1029-10334.
Birts CN, et al.
Sci Signal.
2020 May 5;13(630):eaau9529.
doi: 10.
1126/scisignal.
aau95295.
Leone RD, Powell JD.
Nat Rev Cancer.
2020 Sep;20(9):516-531.
doi: 10.
1038/s41568-020-0273-y.
Epub 2020 Jul 6.
6.
Birts CN.
p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators.
Sci Signal.
2020 May 5;13(630)7.
Xiang, W, et al.
Dietary fats suppress the peritoneal seeding of colorectal cancer cells through the TLR4/Cxcl10 axis in adipose tissue macrophages.
Sig Transduct Target Ther 5, 239 (2020).
On April 7, Nature magazine published an online article entitled "Cell-programmed nutrient partitioning in the tumour microenvironment" (the mechanism of cell-programmed nutrient partitioning in the tumour microenvironment) the study.
This study shows the tumor microenvironment (TME) as a whole function of hyperglycemic aerobic glycolysis, and further shows that the tumor microenvironment with hyperaerobic glycolysis plays an important role in the immune escape and progression of tumors.
.
TME, mainly composed of tumor cells, surrounding immune and inflammatory cells, tumor-related fibroblasts, and nearby interstitial tissues, capillaries, and various cytokines and chemokines, is a complex integrated system.
The earliest discovery of sugar phagocytosis in tumor tissues: Warburg effect In the 1920s, the Nobel Prize winner in Physiology and Medicine, German biochemist Otto Heinrieh Warburg, measured the inflow of normal tissue and tumor tissue into arteries and outflow veins in animals Changes in blood sugar have found that even in an environment with adequate oxygen supply, tumor tissues are more inclined to obtain energy through glycolysis.
Application of Glycophagocytosis in Tumor Tissue: FDG-PET In 2009, Professor Vander published a paper in Science, which further confirmed the existence of the Warburg effect and its importance to the growth of tumor cells.
Taking advantage of the high glucose uptake characteristics of tumors, a method (FDG-PET) for tumor diagnosis and treatment effects was developed.
He also believes that dietary supplementation and strict glucose control can help treat tumors.
Tumor tissue sugar phagocytosis research: the heat will not decrease in 2020, and the exploration of the mechanism is beginning to dawn.
In 2020, Science Signaling and Nature Review Cancer have successively published articles to further clarify the mechanism of tumor Warburg effect, and explore the specificity of various gene mutations or autoimmune functions and tumor cells The relationship between sex metabolism helps to better develop tumor treatment methods or enhance the efficacy of drugs.
In November 2020, Sci signal published the research results of Professor Birts' team.
Professor Birts used a human breast cancer cell model to explore the relationship between the tumor suppressor gene p53 and aerobic glycolysis in cancer cells.
P53 is a key gene that regulates metabolic balance and reduces cell damage under metabolic imbalances.
Due to the lack of mature blood supply in tumors and the gradual increase in aerobic glycolysis, lactic acid accumulates, which leads to acidification of TME and inhibits LDH, which leads to tumor cells.
The ratio of internal NADH:NAD+ increases.
This can cause mutations in p53, which regulates glycolysis of tumor cells, promote metabolic imbalance, and further increase the level of aerobic glycolysis of tumor cells, so that tumor cells continue to proliferate in an environment of metabolic imbalance, and high-speed proliferation promotes survival of tumor cells The screening and iteration of the tumor led to the further progress of the tumor.
NADH-CtBP-p53 pathway regulates glycolysis homeostasis model tumor tissue glycophagocytosis 2021 Nature study: Cancer cells in the tumor microenvironment take up 2/3 of glucose, and bone marrow cells take up the other 1/3.
The latest nature study is demonstrated by using PET Tracer to locate and measure specific cell subpopulations in TME to study glucose uptake.
The study further confirmed that the ability of TME to take up glucose is much better than that of normal tissues.
At the same time, it was found that the glucose uptake of individual immune cells in TME was higher than that of tumor cells, but in terms of TME as a whole, tumor cells were still the cell population with the highest sugar addiction.
The researchers multiplied the glucose uptake of each cell by the number of cells of each type, and found that cancer cells (CD45-) accounted for about 2/3 of the total glucose uptake, myeloid immune cells (CD11B+) accounted for the other 1/3, and other immune cells The contribution of cells (CD3+ and other CD45+) is negligible.
Tumors take up more glucose than normal tissue cells.
Cancer cells in tumor tissues take up more glucose as a whole.
(Note: In the text, CD45- cells are mainly cancer cells, CD45+ cells are immune cells, CD11B+ cells are myeloid immune cells, and CD3+ cells are T Cells) In the study, CD45+ flow cytometry was used to isolate CD11B+ labeled myeloid cells.
Compared with other CD45+ cells, myeloid cells (mainly macrophages) have the highest levels of glucose uptake.
Myeloid immune cells (macrophages) in TME can be divided into M1 type and M2 type macrophages.
M1 type macrophages can kill tumor cells and inhibit tumor cell growth through phagocytosis and mediate Th1 response; M2 type macrophages can promote tissue repair, blood vessel formation, and immunity by producing cytokines and mediating Th2 response Inhibition further contributes to the evolution of tumors.
At present, more and more studies have found that the expression of glycolytic transcription genes in tumor cells can induce TME immunosuppression and directly induce immunosuppressive myeloid cell aggregation.
That is, the specific microenvironment of the tumor forces the phenotype of the macrophages entering the tumor to evolve in a direction that is beneficial to the development of the tumor, that is, the production of M2 macrophages.
Based on this, it can be inferred that macrophages that take up a large amount of glucose in TME will promote their continuous transition to M2 type under a large amount of glucose supply and aerobic glycolysis, thereby promoting tumor progression.
TME is a functional whole.
Tumor cells can be regarded as seeds, and other components are regarded as soil.
Tumor cells interact with other components in the environment and evolve together, which promotes the generation of tumors.
High aerobic glycolysis of tumor cells and myeloid cells, a large amount of lactic acid and H+ accumulate in TME, which affects the proliferation, survival, cytotoxicity and cytokine production of infiltrating T cells, destroys the immune balance in TME, and is beneficial to tumor cell immunity Escape and progress.
The role of fat in the tumor microenvironment: A 2020 Nature sub-Journal study suggests that it may promote the conversion of M2 to M1, which is different from focusing on high-sugar supply.
Another recent study focused on the impact of high-fat supply on tumors. In 2020, an animal experiment conducted by Nature’s sub-Journal Signal Transduction and Targeted Therapy showed that a high-fat diet can inhibit the peritoneal dissemination of colorectal cancer (CRC) cells.
The study pointed out that high fat intake can transform macrophages from M2 type to M1-like phenotype, and stimulate TLR4-dependent M1 macrophage activation and phagocytosis in adipose tissue macrophages, further enhancing CD4+ and CD8+ in visceral fat The recruitment (through Cxcl10) and activation (through M1 cytokines) of T cells will ultimately prevent the metastasis and spread of colorectal cancer.
It can be seen that perhaps by increasing the fat-to-energy ratio in the diet, tumor progression can be inhibited and survival rates improved.
High-fat diet promotes the activation of M1 macrophages.
Summary After nearly 100 years of continuous research, scientists have continuously deepened their understanding of tumor metabolism.
Professor Warburg discovered that the uptake of sugar by tumor tissues is more vigorous a hundred years ago.
Today, our research can go deep into the tumor microenvironment and explore the relationship between the metabolism of different cells and the development of tumors.
Finally, I quote Nature, the first sentence of the latest research, to review the essence of the research and development over the past century: "Tumor cells specifically consume glucose through Warburg metabolism, which is the basis of PET tumor imaging.
Tumor infiltrating immune cells also Rely on glucose, and the metabolism of these impaired immune cells in the tumor microenvironment helps tumor cells to achieve immune escape.
" Therefore, we should limit the sugar intake of tumor patients in clinical practice to reduce the impact of sugar metabolism on the development and development of tumors.
. References: 1.
Reinfeld BI, et al.
Cell-programmed nutrient partitioning in the tumour microenvironment.
Nature.
2021 Apr 7.
doi: 10.
1038/s41586-021-03442-1.
Epub ahead of print.
PMID: 33828302.
2.
Warburg O , Wind F, Negelein E.
THE METABOLISM OF TUMORS IN THE BODY.
J Gen Physiol.
1927 Mar 7;8(6):519-30.
doi: 10.
1085/jgp.
8.
6.
519.
PMID: 19872213; PMCID: PMC2140820.
3.
Vander Heiden MG, et al.
Science 2009; 324:1029-10334.
Birts CN, et al.
Sci Signal.
2020 May 5;13(630):eaau9529.
doi: 10.
1126/scisignal.
aau95295.
Leone RD, Powell JD.
Nat Rev Cancer.
2020 Sep;20(9):516-531.
doi: 10.
1038/s41568-020-0273-y.
Epub 2020 Jul 6.
6.
Birts CN.
p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators.
Sci Signal.
2020 May 5;13(630)7.
Xiang, W, et al.
Dietary fats suppress the peritoneal seeding of colorectal cancer cells through the TLR4/Cxcl10 axis in adipose tissue macrophages.
Sig Transduct Target Ther 5, 239 (2020).
