Ribose in cancer prevention -
Waddell , Maria Raitses-Gurevich , Chani Stossel , Yulia Glick Gorman , Dikla Atias , Charles J. Yeo , Jordan M. Winter , Kenneth P. Olive , Talia Golan , Michael J.
Pishvaian , Donald Ogilvie , Dominic I. James , Allan M. Jordan , Jonathan R. Brody; Poly ADP Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer.
Cancer Res 1 September ; 79 17 : — Patients with metastatic pancreatic ductal adenocarcinoma PDAC have an average survival of less than 1 year, underscoring the importance of evaluating novel targets with matched targeted agents. We recently identified that poly ADP ribose glycohydrolase PARG is a strong candidate target due to its dependence on the pro-oncogenic mRNA stability factor HuR ELAVL1.
Homologous repair—deficient cells compared with homologous repair—proficient cells were more sensitive to PARGi in vitro. In vivo , silencing of PARG significantly decreased tumor growth.
PARGi synergized with DNA-damaging agents i. Mechanistically, combined PARGi and oxaliplatin treatment led to persistence of detrimental PARylation, increased expression of cleaved caspase-3, and increased γH2AX foci.
In summary, these data validate PARG as a relevant target in PDAC and establish current therapies that synergize with PARGi.
PARG is a potential target in pancreatic cancer as a single-agent anticancer therapy or in combination with current standard of care. Sign In or Create an Account. Search Dropdown Menu.
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Article Navigation. Translational Science September 03 Poly ADP Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer Aditi Jain ; Aditi Jain. This Site.
Google Scholar. Lebaron C. Agostini ; Lebaron C. Grace A. McCarthy ; Grace A. Saswati N. Chand AnnJosette Ramirez ; AnnJosette Ramirez.
Avinoam Nevler Avinoam Nevler. Joseph Cozzitorto ; Joseph Cozzitorto. Christopher W. Schultz Cinthya Yabar Lowder Cinthya Yabar Lowder. Kate M. Smith ; Kate M. Ian D. Waddell ; Ian D. Maria Raitses-Gurevich ; Maria Raitses-Gurevich. Chani Stossel ; Chani Stossel.
Yulia Glick Gorman ; Yulia Glick Gorman. Dikla Atias X. However, the detailed mechanisms have remained to be fully determined and require to be further explored.
D-ribose cannot be used to counter liver glycogen shortages, whereas ginseng and maca class compounds may be capable of this. Just as combination therapy may be used to treat cancer 25 , it has been indicated that D-ribose may also be used in combination with other drugs to counter physical fatigue.
D-ribose combined with ginseng extract and morphine produced better results compared with either product alone 26 , 27 and exerted long-term anti-fatigue effects Likewise, studies have indicated that D-ribose serves an important role in both patients with fatigue caused by CHF 9 and mental fatigue 29 by regulating the metabolism of high-energy phosphate.
It was also determined that the swimming time of mice treated with D-ribose alone was significantly longer than of those treated with a combination of caffeine and D-ribose According to the measurement of different substances in the gastrocnemius of fatigued mice immediately after swimming, the combined action of D-ribose and caffeine significantly increased the concentration of ATP, ADP and AMP in the gastrocnemius of mice in comparison with those in the D-ribose alone group.
The concentration of inosine monophosphate IMP decreased in the former and increased in the latter. The concentration of AMP in the caffeine alone group increased, but there was no significant difference in IMP.
After three days of recovery, the ADP concentration of the D-ribose alone group decreased and the IMP concentration increased significantly, and the ADP concentration in the combined caffeine and D-ribose group decreased significantly.
The IMP concentration was not significant compared with the same group before the 3 days recovery. These results support the view that D-ribose is essential for fatigue relief.
Insulin is intricately involved in the regulation of blood sugar levels and exogenous insulin is irreplaceable for diabetics 31 , Insulin resistance a lack of response to insulin is the major barrier in the treatment of patients with diabetes Increasing the response of cells to insulin is the goal of the majority of studies on diabetes.
Hong et al 36 indicated that D-ribose reduced fasting blood glucose levels considerably after 10 and 20 days of intraperitoneal injection, suggesting that D-ribose was able to control blood sugar levels by modulating the sensitivity to insulin in mice.
Therefore, on the one hand, D-ribose increased the sensitivity of cells to insulin, but on the other hand, D-ribose is a monosaccharide. After ingestion, it causes an increase in insulin secretion, resulting in an increase in oxidative decomposition of sugars and a decrease in blood glucose levels.
In addition, using an oral glucose tolerance test, the above study also determined that D-ribose rapidly improved glucose tolerance. By measuring serum insulin levels, it was indicated that the serum insulin concentration was significantly increased after 10 or 20 days of treatment with D-ribose and then returned to normal levels.
Although these results indicate that D-ribose may, in part, increase insulin and glucose tolerance, this method may not be applicable to humans due to physiological differences between mice and humans. Both in developed and developing countries, CHF remains a serious health problem and is the leading cause of death worldwide, particularly amongst elderly populations of developed countries A large amount of work has been performed to understand the pathogenesis of CHF and to improve targeted therapeutic medicines 38 , Pauly and Pepine 8 , 12 indicated that D-ribose supplementation is associated with rapid ATP production in cardiac cells under ischemic and hypoxic conditions, and that it may preserve cardiovascular energy levels.
This suggests that D-ribose may effectively increase ATP synthesis and thus its levels, reducing the damage caused by cardiac ischemia and tissue hypoxia. However, D-ribose is not the preferred substrate for cardiac energy production and cannot provide comparable oxidative energy compared with glucose or pyruvate.
D-ribose serves a role in providing PRPP and adenine nucleotide in models of reversible myocardial injury and related hypertrophy and regional infarction The beneficial effects of D-ribose are attributed to ATP supplementation by increasing the availability of PRPP and increasing ab initio ATP synthesis.
As other pathways, such as ion homeostasis, substrate utilization, proteolytic protein degradation, oxidative stress and mitochondrial function are all affected by transient ischemic injury, metabolic supplementation of D-ribose is most favorable when PRPP is the primary limiting factor.
Likewise, Ma et al 40 reported that D-ribose increased ATP concentrations during myocardial ischemia-reperfusion injury in myocardial cells. Of note, inflammation of myocardial cells caused by free radicals and enzymes without oxygen also significantly increased following D-ribose therapy.
The mechanism underlying this is that D-ribose, via increasing the recovery of myocardial energy, reduced the activation of NF-κB by oxygen free radicals, such as hydrogen peroxide, thereby decreasing the expression of chemokines in activated neutrophils and significantly attenuating the activation, infiltration and degranulation of neutrophils, as well as reducing the release of myeloperoxidase in myocardial tissues.
The activity of other myocardial enzymes is significantly reduced, thus significantly reducing the inflammatory response. In addition, D-ribose supplementation may also reduce dobutamine-induced left ventricular ischemic dysfunction, providing a more predictive assessment of function after surgical revascularization.
The prevalence and incidence of diabetes is increasing and has become a major public health concern worldwide However, it is not the disease itself that eventually leads to a decrease in the quality of life, physical impairments or even death of patients with diabetes, but several chronic complications Several clinically used methods may exacerbate the complications of chronic diabetes.
Increased screening of patients is thus required to manage the conditions and a telemedicine project has been suggested to reduce the impairments caused by chronic complications of patients with diabetes and to improve their quality of life However, studies such as that by Salci et al 43 tested preventative measures For example, blood pressure control, psychosocial concerns and detection and treatment of chronic complications for chronic diabetes mellitus complications and the results indicated that they were not sufficiently useful.
This indicates there are various deviations in implementing certain precautionary steps and also demonstrates the nature and difficulty of controlling and treating patients with diabetes There is a requirement for improved methods to diagnose chronic complications in patients with diabetes early and more effectively.
Certain clinicians use glycosylated hemoglobin as a biomarker 45 , A study reported that patients with diabetes had anti-D-autoantibodies against riboglycosylated hemoglobin, which may be used as a marker for early diabetes detection, and inhibition of its output may be used to minimize diabetes progression and the incidence and development of subsequent complications Furthermore, Chen et al 23 also studied the physiological functions of D-ribose in the pathogenesis of type 2 diabetes, suggesting that D-ribose may react with hemoglobin to generate glycosylated hemoglobin.
Of note, the glycated serum protein GSP caused by D-ribose is more effective than other sugars, such as D-glucose. In addition, Chen et al 48 reported that D-ribose may also enhance serum protein glycosylation to produce GSP, leading to a series of complications of chronic diabetes.
The authors also indicated that serum protein glycosylation caused tissue damage in the previous weeks, whereas hemoglobin glycosylation caused tissue damage in the previous weeks. These two types of non-enzymatic glycosylation related tissue damage are the leading causes of the complications of chronic diabetes.
D-ribose may lead to the formation of advanced glycation end products AGE and complications of chronic diabetes, such as diabetic nephropathy Regarding the possible mechanism, as compared with glucose, D-ribose is able to rapidly interact with the amino residues of non-enzymatic protein to form early glycosylation products for instance, reversible Schiff base in patients with diabetes; these early glycosylation products may be further rearranged, dehydrated and condensed to form AGE, which bind to receptors for AGE RAGE , which results in increased expression of vascular endothelial growth factor and vascular cell adhesion factor to enhance vascular permeability, angiogenesis and local inflammation.
Furthermore, the activation of the AGE-RAGE pathway in monocytes may also increase the secretion of various cytokines and cause a series of oxidative stress reactions, so as to serve a role in the chronic complications of diabetes Although D-ribose may lower blood sugar levels over a short period of time, it may also trigger complications of chronic diabetes following long-term accumulation.
The mechanism by which D-ribose is implicated in complications of chronic diabetes is via a D-ribose-induced increase in glycosylated hemoglobin, further resulting in the generation of AGEs.
Therefore, high D-ribose concentrations are associated with chronic diabetic complications. These results indicate that D-ribose is a double-edged sword in the management of diabetes. It may be possible to measure the content of glycosylated proteins or D-ribose in patients with diabetes to predict potential clinical complications and thus introduce effective preventative steps; however, further studies are required to confirm this hypothesis.
As indicated above, the potential importance of D-ribose in two world-leading diseases, CHF and diabetes, is well established. The efficacy of D-ribose in other diseases has also been assessed. The term restless leg syndrome was coined in and was previously known as Willis Ekbom disease since 50 , Restless leg syndrome is characterized by uncomfortable feelings and discomfort, frequently when resting in the lower limbs, followed by an uncontrollable movement for relief.
It is a movement-dominated sensory nerve condition which can cause sleep disorders. This disease severely affects the quality of life of patients and has thus attracted significant attention. It has been indicated that intake of D-ribose does not completely eradicate the symptoms of the disease 52 ; however, it may improve a patient's quality of life, reduce the severity of the effects and prevent disease progression.
The effect of D-ribose, which may rapidly replace ATP in muscle cells, has also been used for the treatment of fibromyalgia and chronic syndrome. Teitelbaum et al 53 and another study 15 reported that D-ribose may significantly alleviate fibromyalgia and chronic symptoms and improve quality of life.
Likewise, Gebhart and Jorgenson 54 indicated that if traditional therapy fails in patients with muscle fiber pain, D-ribose may be considered, which has certain beneficial effects on the disease. Furthermore, according to one study, D-ribose may have cosmetic properties Indeed, D-ribose enhances the metabolism of skin cells and regulates ATP production.
The results were also confirmed by Shecterle and St Cyr D-ribose has numerous applications; however, there are side-effects to its use. Several studies have indicated that administration of certain concentrations of D-ribose in various animal models is healthy and does not cause any adverse effects regarding behavior, hematology, biochemistry, histology or general pathology Thus, it may be hypothesized that D-ribose has beneficial effects on the function of local muscle cells or tissue cells, is able to relieve symptoms and has no apparent toxicity in any area and is thus appropriate for widespread use.
The uses of D-ribose for treating or detecting certain diseases described in detail above have several advantages; however, if the concentration of D-ribose in the body is too high, adverse effects may occur.
The potential implications of high concentrations of D-ribose are discussed in detail below. AGEs may exhibit notable cytotoxic effects, a major cause of chronic diabetes complications Fig. Several studies have also suggested that the clinical complications of type 2 diabetes are related to the accumulation of AGEs and the inflammatory response mediated by RAGE 49 , However, high D-ribose levels are associated with AGE accumulation.
By assessing the impact of D-ribose on human nonenzymatic glycosylation of myoglobin, Yamamoto and Yamamoto 49 determined that D-ribose may accelerate glycosylation of myoglobin and other proteins more efficiently than D-glucose.
Yu et al 62 also suggested that the urine concentration of D-ribose in patients with type 2 diabetes was substantially higher than that of normal individuals, which also indicated high levels of D-ribose in the body of patients with diabetes.
In addition, high D-ribose concentrations may also cause chronic diabetes complications by other means. Thus, high concentrations of D-ribose may be a cause of the complications of chronic diabetes Fig. D-ribose may cause a variety of chronic complications, such as nervous system-related diseases and diabetic nephropathy.
How D-ribose causes these chronic complications is discussed further below. Dual roles of D-ribose: Therapeutic implications and side effects.
AGEs, advanced glycation end products. Schematic of the pathological processes of D-ribose-induced diabetes.
On the other hand, the presence of a high concentration of D-ribose, which can act as an activation signal, leads to the release of NLRP3 inflammatory bodies from lysosomes following the activation of NLRP3 inflammatory bodies, thereby promoting the occurrence of diabetic kidney disease.
This is caused by the gradual renal fibrosis which is induced by the release of the pro-inflammatory cytokine IL-1β.
Additionally, D-ribose can also lead to the glycosylation of HbAlc and AGEs, that both contribute to the development of diabetic associated complications. AGEs, advanced glycation end products; NLRP3, nucleotide-binding oligomerization domain-like receptor family protein 3.
Alzheimer's disease is a disorder of the central nervous system characterized by progressive cognitive dysfunction and behavioral impairment. It is a common disease amongst the elderly, results in severe memory losses and renders an individual unable to socially function properly. It has become a significant issue impacting global public health systems and sustainable social growth.
In the course of researching the pathogenesis and treatment of Alzheimer's disease, several scientists have identified a certain association between D-ribose and Alzheimer's disease. Javed et al 64 studied the pathogenesis of Alzheimer's disease caused by D-ribose and indicated that detecting D-ribose concentrations in the plasma may help doctors to better characterize the disorder.
Han et al 65 inferred that excessive D-ribose concentrations increased the levels of glycosylated proteins and accumulation of AGEs in mice, resulting in corresponding cytotoxicity.
Wei et al 66 reported that D-ribose induced protein misfolding and aggregation faster than other monosaccharides and induced apoptosis in SHSY5Y neural cells. The results indicated that D-ribose may affect certain age-associated diseases.
Studies have also suggested that uncontrolled diabetes may increase the risk of Alzheimer's disease and vascular dementia In addition, D-ribose serves an important role in type 2 diabetic encephalopathy.
D-ribose has been demonstrated to cause the rapid saccharification of α-synuclein to form a molten spherical polymer, leading to oxidative stress and high cytotoxicity It was hypothesized that diabetic encephalopathy is linked to D-ribose-induced Tau protein glycosylation To test this hypothesis, Wu et al 70 examined age-related cognitive decline and diabetic encephalopathy using intragastric long-term D-ribose administration in mice to induce type 2 diabetic encephalopathy.
The results indicated that D-ribose glycosylation was enhanced. In addition, it has been shown in a previous study that AGEs were able to inhibit brain-derived neurotrophic factor expression and tropomyosin-associated kinase B, resulting in hyperphosphorylation of the Tau protein.
It is therefore proposed that selective inhibition of ribose glycosylation may be used as a therapeutic strategy for the prevention of Alzheimer's disease and type 2 diabetic encephalopathy Wang et al 72 also indicated that in alkaline environments, D-ribose may decompose to formaldehyde by the reverse aldol reaction, and that by determining the content of formaldehyde in various parts of mice, it was suggested that formaldehyde produced by D-ribose accumulates in the brain of the mice and that the accumulation of endogenous formaldehyde to pathological concentrations may lead to disturbance of consciousness and cognition.
However, it was also hypothesized that accumulation of D-ribose-induced AGEs is an important means underlying the occurrence and development of diabetic encephalopathy Han et al 65 reported that D-ribose glycosylation led to the accumulation of AGEs in the nervous system, leading to spatial cognitive impairment and astrocyte-mediated RAGE-dependent inflammation.
This indicates that D-ribose-induces cognitive dysfunction linked to type 2 diabetic encephalopathy The study by Gheith et al 74 agreed with this hypothesis and proved that the accumulation of AGEs may lead to neuronal dysfunction and death.
According to a recent study, high levels of D-ribose in type 1 diabetes may suggest that D-ribose is involved in complications associated with type 1 diabetes, including encephalopathy Several of the above studies have indicated possible damage to the nervous system caused by high concentrations of D-ribose in the body and provided an alternate means of understanding the potential pathogenesis of Alzheimer's disease and diabetic encephalopathy.
Whether Alzheimer's disease and diabetic encephalopathy may be prevented or delayed by reducing the concentration of D-ribose or by cutting off the D-ribose pathway involving glycosylation of related proteins and generation of AGEs remains to be determined.
To assess this, additional in-depth studies, novel treatment agents and clinical trials are required. Diabetic nephropathy is one of the most severe diabetic complications and a leading cause of end-stage renal disease worldwide. Therefore, research on the pathogenesis and care for diabetic nephropathy has gained increasing attention from numerous academics, including analysis of poly ADP-ribose polymerase-1 PARP Various experiments have suggested that inhibiting PARP-1 is able to prevent or alleviate diabetic nephropathy 75 , Furthermore, it has been indicated that inhibiting aldose reductase activity was also able to minimize nitrosation stress and PARP activation of glomerular mesangial cells in a high-glucose environment Studies on sodium-glucose transporter-2 SGLT-2 and its involvement in renal tubules have also been performed.
It has been indicated that SGLT-2 inhibition combined with renin-angiotensin system therapy inhibition was able to better protect the long-term health of the kidney and help delay the development of renal diseases in patients with type 2 diabetes 78 , Furthermore, an increasing number of studies are assessing the pathways that underlie AGE-mediated diabetic nephropathy 80 , 81 and the AGE-RAGE-oxidative stress system theory Several studies have indicated increased expression of RAGE in advanced chronic kidney disease, which indirectly demonstrates the close relationship between AGEs and diabetes The increase in AGE-modified plasma proteins is associated with the production of ROS caused by RAGE, the activation of transcription factor NF-κB and the pathological changes in gene expression levels in several cell types It is well established that D-ribose influences the incidence and development of diabetic nephropathy via AGE accumulation.
To confirm this point, Zhang et al 85 used murine mesangial cells as an experimental model. They indicated that D-ribose induced nonenzymatic glycosylation of related proteins and led to the accumulation of AGE-induced glomerular cell dysfunction.
Increasing D-ribose concentrations may also lead to increased ROS and cytokine levels, leading to podocyte inflammation and renal fibrosis.
In addition, Hong et al 36 formulated the AGE-RAGE-oxidative stress system theory and other mechanisms by which D-ribose causes diabetic nephropathy.
One approach was the induction of both exogenous and endogenous D-ribose to form and distinguish NOD-, LRR- and pyrin domain-containing protein 3 inflammatory bodies in podocytes and to secrete podocytes via extracellular vesicles EVs.
Therefore, releasing cytokine IL-1β may trigger glomerular injury, and D-ribose may also reduce interactions between lysosomes and multivesicular bodies MVBs , increase the fusion of MVBs and plasma membrane and increase cytokine IL-1β release via EV secretion.
Another potential mechanism is the increase of the D-ribose content of ceramide in the lysosome to control the lysosome-ceramide sphingolipid mechanism of interaction with MVBs, enhancing the ability of podocytes to release EVs and increasing the release of IL-1β to enhance the inflammatory response Together, in addition to daily blood sugar regulation, patients with diabetes should consider monitoring the concentration of D-ribose daily to avoid diabetic nephropathy.
This may improve the quality of life of patients with diabetes. Currently, research on the clinical use D-ribose is still in the relatively early stages and a considerable amount of further investigation is required. However, based on the body of literature available, it is well established that D-ribose has several and broad prospects in various areas, including medicine and healthcare, as well as sports and athletics.
For instance, in emergencies, such as during myocardial ischemia-reperfusion injury caused by cardiac operations or cardiac arrest, D-ribose may directly accelerate PRPP synthesis, thereby rapidly increasing the ATP concentration and other mechanisms in myocardial cells by injecting a certain amount of D-ribose to reduce the occurrence of myocardial ischemic injury.
At the same time, further research and confirmation of the appropriate concentration ranges of D-ribose to use during these procedures and whether it may be used in conjunction with other first-aid rescue medications, such as those for cardiac arrest, is required.
Furthermore, a series of existing studies on the relationship between D-ribose and diabetes indicated that the concentration of D-ribose in patients with diabetes is proportional to the incidence and severity of diabetic complications.
For the majority of people with diabetes, the primary factors impacting the quality of life or reducing their lifespan is not diabetes itself, but the resulting complications. Whether D-ribose may be used as a medication to treat diabetic complications and the effects of the D-ribose concentration on the body should be further studied.
Simultaneously, improving D-ribose concentration determination technologies is particularly important. Thus, assessing D-ribose concentrations in patients with early diabetes may be used to predict the probability and extent of diabetic complications.
In addition, reducing D-ribose intake in everyday life in patients with diabetes may be of direct significance. Perhaps, D-ribose analogues or drugs that target D-ribose may be used in advance to minimize patient harm from diabetic complications and reduce the occurrence of diabetic complications.
Ultimately, D-ribose may be used to improve the quality of life of patients with diabetes and extend their lifespan. Finally, D-ribose is also used as an anti-fatigue medication to enhance muscle exercise intensity in athletes and is commonly used as a food additive in food and health products.
However, there is still no definitive conclusion on its safe range. In addition, whether excessive use of D-ribose poses other potential health hazards, as well as whether D-ribose is suitable for everyone requires further study. This study was supported by the Hunan Provincial Natural Science Foundation of China grant no.
SL, JW, YX and LZ contributed to the conception of the study and wrote the manuscript. HQ and MN contributed towards the conception of the study and revised it critically for important intellectual content. JF, NY and ZZ contributed to the preparation of the manuscript and illustration of the figures.
All authors read and approved the final manuscript and agreed to be accountable for all aspects of the work. Bailey JM: The consequences for amino acid homochirality if L-ribose RNA and not D-ribose RNA had evolved first.
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Ribose kn a carbohydrate vital Natural anti-aging remedies the body's manufacture of ATP adenosine canncerwhich is canceer major ni of energy used by our cells. Quite a Nutritional guidelines for body fat percentage reduction studies have been done on ribose, kn Ribose in cancer prevention to its potential usefulness for individuals with heart disease. When the heart is starved for oxygen, as can occur with a heart attack or anginait loses much of its ATP, and its ATP levels remain low for several days, even after blood flow is resumed. This finding has raised hopes that ribose supplements might improve heart functioning and increase exercise capacity. Ribose is better known as a sports supplement. June Ribpse,by Carmen Phillips. Cnacer Importance of water for athletes no Weight loss supplements to prevenhion the energy pancreatic cancer cells need to survive and grow, they can use another molecule called Ribose in cancer prevention. A new study has revealed some important information about the cancet of one of the most notorious forms of cancer. Pancreatic cancer, the study found, can readily turn to an alternate source of energy to survive when its primary source, the sugar molecule glucoseis in short supply. Tumors in the pancreas typically develop a dense, nest-like structure around them—an area often referred to as the tumor microenvironment —and they also often lack intact blood vessels. This unruly architecture surrounding these tumors creates conditions that decrease the supply of glucose, an essential fuel source for normal and cancer cells.
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