Scientists have made new achievements in the field of cancer metabolism!

In !-- article, we've compiled and shared recent scientific achievements in the field of cancer metabolism research! Photo Credit: University of California San Diego 1 Nature: How can you effectively slow tumor growth and progress by easily pressing a metabolic switch? Doi:10.1038/s41586-020-2609-x In a recent study published in the international journal Nature, scientists from the University of California and other institutions found that enzymes called serine palmitoyl-transferase (SPT, serine palmitoyl-transferase) can act as a metabolic reaction switch to inhibit tumor growth.
By limiting dietary amino acids serine and glycine, or pharmacologically targeted synthase-phosphate glycerine dehydrogenase, researchers can induce tumor cells to produce a toxic lipid that slows the progression of tumors in mice, and later researchers need to conduct further studies to determine whether this method can be converted into clinical patients.
Over the past 10 years, scientists have found that removing serine and glycine from animal diets may slow the growth of certain tumors, but most researchers have focused on how these diets affect the apparent genetics, DNA metabolism, and antioxidant activity of DNA.
researcher Professor Christian Metallo said the study highlighted the complexity of metabolism and the importance of understanding physiological characteristics across many different bio-chemical pathlines when considering the use of metabolic therapies.
: Cell Metabol: Breakthrough! Scientists may be expected to target metabolic changes in acting cells to remove drug-resistant cancer cells! doi:10.1016/j.cmet.2020.07.009 Chemotherapy can effectively treat blood cancers such as leukemia, but drug-resistant cancer cells tend to avoid the most primitive drug treatment strategies to promote cancer recurrence, a study has published In a study published in the international journal Cell Metabolism, scientists from Harvard University and others identified the unique characteristics of drug-resistant cancer cells, namely, the short-term changes in their metabolic processes (how nutrients are used), and the findings could help researchers develop new ways to target the metabolic path paths that act on cancer cells to effectively eliminate drug-resistant cancer cells.
researcher David Scadden said: 'In the field of cancer research, we generally believe that drug resistance is associated with permanent genetic changes, and in this study we found that some cancer cells may also use other mechanisms to survive chemotherapy, others do not, including how cancer cells use nutrients in the microencess, and the way they use nutrients may be as important as the genetic background they have.'
Drug-resistant cancer cells are so rare that it is often difficult for researchers to detect them after chemotherapy, and in order to be able to identify drug-resistant cancer cells and track their progress over time, the researchers used a mouse model of acute myeloid leukemia to mark bioluminescent and fluorescent proteins on cancer cells, which were then analyzed at two special points in time.
(3) eLife: Blocking sugar metabolism or effectively slowing the progression of lung cancer Doi:10.7554/eLife.53618 In a study published in the international journal eLife, scientists from the Federal Institute of Technology in Lausanne, Switzerland, and others have found that blocking a pair of glycolytic proteins may be an effective treatment for lung cancer.
Cancer cells can grow and spread quickly with large amounts of sugar, forcing scientists to cut off sugar supplies as a new treatment for cancer, which current research suggests may be an effective treatment but must be blocked in multiple ways at the same time.
glucose transporters provide sugar to cells, making it a new target to help researchers develop new ways to starve cancer cells, but researchers don't yet know the best way, or whether cancer cells switch to other sources of energy to grow and spread.
: Tumor metabolites hinder DNA repair! The reason is local chromosomal signal disturbance! Doi:10.1038/s41586-020-2363-019 At the end of the century, chromosomal abnormalities detected under the optical mirror revealed a large-scale genomic instability that led to abnormal chromosome numbers for certain types of cancer.
, biochemist Otto Warburg observed that tumor cells tend to use different pathways of glucose and energy metabolism than normal cells.
we now know that genomic instability and metabolic changes are two common features of most tumor cells.
genetic instability has been studied since its discovery; metabolic changes have only recently been rediscoed as a field of study.
the interaction between the two processes in cancer treatment has not been reported so far.
June 4th, Sulkowski et al., published in the journal Nature, revealed how several metabolites that accumulate high levels in tumor cells inhibit DNA repair, revealing a direct link between metabolic changes and genomic instability caused by DNA damage.
mutations in genes that encode iso-citric acid dehydrogenase 1 and 2 (IDH1 and IDH2) cause cells to accumulate high levels of metabolites 2-hydroxypropyl dichloride (2-HG).
the genes that encode Yanhuso acid hydrase and amber acid dehydrogenase mutate, causing cells to accumulate high levels of Yanhuso acid and amber acid molecules, respectively.
these three small molecules are often referred to as tumor metabolites because their accumulation promotes tumor development, and they are structurally similar to the molecular alpha-ketone diac acid (alpha-KG).
this is an intermediate product of the Krebs cycle path, also known as a component, called a common substrate, a class of substances called alpha-KG/Fe (II) that is necessary to function in the form of a double oxygenase.
!--/ewebeditor:page--!--ewebeditor:page-title"--5" Nat Cell Biol: Breast cancer cells may be able to change their metabolic strategies to metastasize doi:10.1038/s 41556-020-0477-0 In a recent study published in the international journal Nature Cell Biology, scientists from the University of California and other institutions are promising to develop new strategies to prevent cancer cells from spreading to other organs of the body and effectively reduce mortality in breast cancer patients.
researchers say breast cancer cells can convert metabolic strategies to metastasis, not using glucose as energy, but using mitochondrial metabolism for a limited time; Devon A. This may have important potential clinical implications, Dr. Lawson said, because drugs that target mitochondrial metabolism may be effective in suppressing the spread of cancer in breast cancer patients; tumors are often thought to contain abnormally functional mitochondrials and are often maintained by anaerobic enzymes or Wahlberg metabolism, a theory challenged by the study' findings that cancer cells can spread by mitochondrial metabolism during breast cancer.
images: Jeroen Claus (Phospho Biomedical Animation) 6: A deep understanding of how scientists are looking for new associations in cancer metabolism! News read: Searching for novels connections in cancer metabolism Imagine that there is now a row of dominoes, when one is knocked down, the rest will roll down together, the same is true of cancer, when a cell begins to develop cancer, the important cell path will be changed, which is like a chain reaction, when a point in the path is mutated, the downstream will be affected, as if dominoes.
path paths that are destroyed in cancer regulate the way cells acquire or process energy, i.e. their metabolism.
While researchers know a lot about the errors that disrupt metabolic path path pathogenesis in cancer, there is not much research linking these mutations to the mechanisms of cell behavior; researcher Dr. George Poulogiannis, who studies the association between cell metabolism, cancer and diet, says finding new associations in cancer metabolism may help researchers better understand the pathogenesis of cancer and develop new, more targeted therapies.
to solve such a complex puzzle, researchers need a rather unique tool.
To assess metabolic changes in cancer cells, researchers have developed a tool called iKnife, an electro-surgical device that can sniff out cancer during surgery and has been tested for breast and ovarian cancer, explains Poulogiannis, a researcher who a few years ago introduced a very simple-thinking technique that connects electronic surgical devices to mass spectrometers and determines the ionology properties of smoke that is being produced.
7 Dev Cell: Revealing the regulatory pathways of pancreatic cancer cell drinking helps target cancer cell metabolism and prevents cancer cells from growing doi:10.1016/j.devcel.2019.05.043 Because of the urgent need for nutrients, fast-growing pancreatic tumors seek "fuel" through another way -- cell drinking.
scientists hope to stop the process, commonly known as "cell drinking," which could lead to cancer hunger drugs.
, the first thing that is needed is basic information -- such as invisible molecular signals that drive the process.
Recently, scientists from the Sanford Burnham Prebis Institute of Medicine have identified a signaling path that regulates cell drinking, a nutritional clue that triggers tumor growth processes and key metabolic differences, revealing new directions in drug development and patient treatment.
results were published in the journal Developmental Cell.
To find the Achilles heel of pancreatic cancer metabolism, we need to have a better understanding of how these tumors get nutrition," said senior author Dr. Cosimo Commisso, senior author of the paper and assistant professor at the Sanford Burnham Prebis Institute of Medicine's Cancer Center.
" study shows that, like humans, the metabolism of pancreatic cancer is varied.
some pancreatic tumors can be "up" or "downgraded" by cells, depending on the availability of glutamine.
is an amino acid that plays a key role in the metabolism of fast-growing cells.
other tumors naturally have high levels of cell drinking.
we have also identified molecular regulatory factors for this process, which may eventually lead to personalized therapy.
"8" Cancer Res: Metabolic adaptability guarantees the survival of cancer cells doi:10.1158/0008-5472.CAN-19-0650p53 is one of the most important control proteins in cell growth, and colon cancer cells lacking p53 activate specific metabolic pathways to accommodate the lack of oxygen and nutrients inside the tumor.
as scientists at the German Cancer Research Centre (DKFZ) have now discovered, statins commonly used to lower cholesterol block this metabolic pathway and cause cancer cells to die.
now, researchers plan to study this potential treatment in more detail in cancer cells and animal experiments.
once the tumor reaches a certain size, cancer cells face a particular challenge: growing in a tissueless manner, and the tumor lacks blood vessels, which leads to a lack of oxygen and nutrients inside the tumor.
, a metabolic expert at DKFZ, explains: "Cancer cells must completely recombine all their metabolisms to accommodate this defect.
" Schulze points out that important control proteins and tumor suppressors p53 play a vital role in adapting to defects.
, the authors and others examined colon cancer cells that lacked p53 to see how p53 actually affected metabolic adaptation.
. Nature: Secret doi:10.1038/s41586-019-1678-1 A new study led by researchers at the University of Chicago reveals why cancer cells consume and use nutrients differently from healthy cells, and how this difference promotes the survival and growth of cancer cells.
all cells need to produce energy to sustain life, but the need for energy for cancer cells to grow and multiply rapidly is increasing.
understanding how different types of cells self-sustain or metabolize is an attractive area of research, as this process can be interrupted and exploited by the development of new drugs.
, metabolism also plays a role in the regenerative nature of immune cells.
for decades, biologists have been trying to shed light on the complexity of how cell metabolism affects their function.
study, published in the journal Nature, showed that lactic acid, a final product of metabolism, alters the function of macrophages and thus their behavior.
!--/ewebeditor:page--!--ewebeditor:page"--lactic acid is the end product of the Warburg effect and has long been considered a metabolic waste.
recent studies have shown that lactic acid regulates the function of many cell types (immune cells and stem cells).
, lactic acid is not only not a waste, but may also be a key regulator affecting cell function.
in recent years, despite the achievement.