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Urolithin A is a gut metabolite of ellagitannins and reported to confer health benefits, e.g., by increased clearance of damaged mitochondria by macroautophagy or curbed inflammation. One targeted cell type are macrophages, which are plastic and able to adopt pro- or anti-inflammatory polarization states, usually assigned as M1 and M2 macrophages, respectively. This flexibility is tightly coupled to characteristic shifts in metabolism, such as increased glycolysis in M1 macrophages, and protein expression upon appropriate stimulation. This study aimed at investigating whether the anti-inflammatory properties of u rolithin A may be driven by metabolic alterations in cultivated murine M1(lipopolysaccharide) macrophages. Expression and extracellular flux analyses showed that urolithin A led to reduced il1β, il6 , and nos2 expression and boosted glycolytic activity in M1(lipopolysaccharide) macrophages. The pro-glycolytic feature of urolithin A occurred in order to causally contribute to its anti-inflammatory potential, based on experiments in cells with impeded glycolysis. Mdivi, an inhibitor of mitochondrial fission, blunted increased glycolytic activity and reduced M1 marker expression in M1(lipopolysaccharide/ urolithin A), indicating that segregation of mitochondria was a prerequisite for both actions of urolithin A. Overall, we uncovered a so far unappreciated metabolic facet within the anti-inflammatory activity of urolithin A and call for caution about the simplified notion of increased aerobic glycolysis as an inevitably proinflammatory feature in macrophages upon exposure to natural products. [ABSTRACT FROM AUTHOR]

Urolithin A is a gut metabolite of ellagitannins and reported to confer health benefits, e.g., by increased clearance of damaged mitochondria by macroautophagy or curbed inflammation. One targeted cell type are macrophages, which are plastic and able to adopt pro- or anti-inflammatory polarization states, usually assigned as M1 and M2 macrophages, respectively. This flexibility is tightly coupled to characteristic shifts in metabolism, such as increased glycolysis in M1 macrophages, and protein expression upon appropriate stimulation. This study aimed at investigating whether the anti-inflammatory properties of u rolithin A may be driven by metabolic alterations in cultivated murine M1(lipopolysaccharide) macrophages. Expression and extracellular flux analyses showed that urolithin A led to reduced il1β, il6 , and nos2 expression and boosted glycolytic activity in M1(lipopolysaccharide) macrophages. The pro-glycolytic feature of urolithin A occurred in order to causally contribute to its anti-inflammatory potential, based on experiments in cells with impeded glycolysis. Mdivi, an inhibitor of mitochondrial fission, blunted increased glycolytic activity and reduced M1 marker expression in M1(lipopolysaccharide/ urolithin A), indicating that segregation of mitochondria was a prerequisite for both actions of urolithin A. Overall, we uncovered a so far unappreciated metabolic facet within the anti-inflammatory activity of urolithin A and call for caution about the simplified notion of increased aerobic glycolysis as an inevitably proinflammatory feature in macrophages upon exposure to natural products. [ABSTRACT FROM AUTHOR]

The article offers information on the complex relationship between diet, sugar consumption, and cancer risk. As lead line, it highlights that understanding cancer processes and predicting susceptibility remains challenging. Topics include the impact of ultra-processed foods on cancer mortality rates, the association between sugar consumption and cancer risk, and recent research uncovering how sugar metabolism influences cancer development.

The article discuses the role of solid state sensors in activation of immune cell metabolism. It is reported that measurement of cell metabolism at different stages of cell therapy manufacturing can provide incisive and quantitative information about metabolic poise and potency of the cells. It is further reported that tools such as the Seahorse XF Pro Analyzer provides incisive information about critical quality attributes of immune cells throughout therapeutic design and manufacturing.

A recent preprint abstract discusses a new technology called Sorting by Interfacial Tension (SIFT) that allows for the sorting of cells based on their glycolytic levels. This passive and label-free droplet microfluidic platform uses interfacial tension to sort droplets containing single cells into two populations based on pH. The SIFT technique is expanded by exploiting dynamic droplet acidification, allowing for the isolation of cells with distinct glycolytic levels. This technology has potential applications in oncology, immunology, and immunotherapy. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

According to a preprint abstract, researchers have used a CRISPR approach to study the roles of mitochondrial fission and fusion in aging neurons. They found that fusion is more important than fission for maintaining long-term neuronal function. Neurons can survive chronic mitochondrial fragmentation by triggering a cancer-like response, which includes upregulation of the gene Lactate dehydrogenase. These findings provide insights into the relationship between neuronal metabolism, aging, and neurodegeneration. However, it is important to note that this preprint has not yet been peer-reviewed. [Extracted from the article]

The article reports on research from Washington University regarding the use of nanoparticles to target neutrophil glycolysis in preventing lung ischemia-reperfusion injury. Topics include the development of lipid nanoparticles conjugated with a glycolysis flux inhibitor, the high specificity of these nanoparticles for neutrophils, and their effectiveness in reducing injury and inflammation in the lung after transplantation.

The article details research from Zhejiang University revealing that acidic pepsin enhances the growth and invasion of laryngeal carcinoma cells by increasing Glut-1 expression and promoting glycolysis. Topics discussed include the impact of acidic pepsin on Glut-1 and glycolysis, its effect on cancer cell viability and migration, and the role of glycolytic inhibitors in reversing these effects.

The article discusses research from the Department of Pulmonary and Critical Care Medicine, focusing on the role of circ_UBE2C in the proliferation and glycolysis of lung cancer cells through its regulation of the miR-107/HK2 axis. Topics discussed include the correlation between circ_UBE2C, miR-107, and HK2 expression in lung cancer, their impact on patient survival, and the effects of knocking down circ_UBE.

A study conducted by researchers at Henan University of Chinese Medicine in China explored the potential therapeutic effects of a Chinese herbal compound called Huanshaodan (HSD) on Alzheimer's disease (AD). The researchers investigated whether HSD could regulate the metabolic reprogramming of microglial cells through the mTOR/HIF-1a signaling pathway to alleviate neuroinflammation in AD. The study found that HSD improved cognitive impairment and reduced amyloid-beta deposition in mice with AD. It also suppressed glycolysis and neuroinflammation in both mice and BV2 cells, and these effects were reversed by an mTOR agonist. The findings suggest that HSD may have anti-AD effects by regulating microglial glucose metabolism. [Extracted from the article]

A new study conducted by researchers at the First Affiliated Hospital of Soochow University explores the prognosis of pancreatic cancer based on glycolytic and hypoxic metabolic subtypes. The study analyzed mRNA, SNP, and clinical data from The Cancer Genome Atlas (TCGA) and identified four subtypes. The glycolytic subtype was associated with longer survival and better response to chemotherapy and immunotherapy compared to the hypoxic subtype. The study suggests that alterations in genes involved in glycolysis and hypoxia affect the prognosis of pancreatic cancer. [Extracted from the article]

A recent study conducted by Fudan University Shanghai Cancer Center has provided new insights into colon cancer. The study focused on the role of a protein called UBTD1 in colorectal cancer (CRC) progression. The researchers found that UBTD1 expression was significantly higher in cancer tissue compared to adjacent normal tissue, and higher expression was associated with poorer survival and more lymph node metastasis. The study also revealed that UBTD1 promotes CRC progression by upregulating glycolysis through the b-TrCP/c-Myc/HK2 pathway. These findings suggest that UBTD1 could serve as a prognostic biomarker and therapeutic target in CRC. [Extracted from the article]

The lichen compound protolichesterinic acid (PA) has an anti-proliferative effect against several cancer cell lines of different origin. This effect cannot be explained by the known inhibitory activity of PA against 5- and 12-lipoxygenases. The aim was therefore to search for mechanisms for the anti-proliferative activity of PA. Two cancer cell lines of different origin, both sensitive to anti-proliferative effects of PA, were selected for this study, T-47D from breast cancer and AsPC-1 from pancreatic cancer. Morphological changes were assessed by transmission electron microscopy, HPLC coupled with TOF spectrometry was used for metabolomics, mitochondrial function was measured using the Agilent Seahorse XFp Real-time ATP assay and glucose/lactate levels by radiometry. Levels of glutathione, NADP/NADPH and reactive oxygen species [ROS] were measured by luminescence. Following exposure to PA both cell lines showed structural changes in mitochondria that were in line with a measured reduction in oxidative phosphorylation and increased glycolysis. These changes were more marked in T-47D, which had poorer mitochondrial function at baseline. PA was processed and expelled from the cells via the mercapturic pathway, which consumes glutathione. Nevertheless, glutathione levels were increased after 24 hours of exposure to PA, implying enhanced synthesis. Redox balance was not much affected and ROS levels were not increased. We conclude that PA is metabolically processed and expelled from cells, leading indirectly to increased glutathione levels with minimal effects on redox balance. The most marked effect was on mitochondrial structure and metabolic function implying that effects of PA may depend on mitochondrial fitness. [ABSTRACT FROM AUTHOR]

The article focuses on research into the metabolism of cancer cells and alternative methods of fighting cancer. It comments on biochemist Otto Warburg's observation in 1924 that changes in cell metabolism defined cancer and could provide a mechanism to defeat it. It mentions up to 80 percent of cancers generate energy through aerobic glycolysis and if the enzyme needed for the final reaction is inhibited, tumors shrink. It mentions the role of glucose and lactate in cancer cell metabolism.

This article discusses a study led by Prof. Yi Bai, Prof. Haojian Zhang, and Prof. Liang Kong, which explores the role of epigenetic regulation in skeletal stem cell (SSC) quiescence and potency during skeletogenesis. The researchers used flow cytometric analysis and epigenetic and transcriptomic analyses to map the developmental trajectory of SSCs. They identified Ptip as a critical chromatin modifier that determines SSC identity and found that loss of Ptip disrupts SSC function and leads to bone dysplasia. Additionally, they discovered that Ptip suppresses glycolysis in SSCs, and inhibiting glycolysis improves SSC function. These findings provide new insights into the epigenetic regulation of SSCs and may have implications for the treatment of bone developmental disorders. [Extracted from the article]

A recent study conducted at University Hospital Grenoble Alpes in France has found that despite the use of desensitization strategies in kidney transplant recipients, there is still a risk of antibody-mediated rejection. The study included 10 highly sensitized recipients who underwent desensitization therapy prior to transplantation. The researchers observed a decrease in donor-specific antibodies and certain B-cell subsets, but found that memory B cells and plasma cells persisted even up to 12 months after transplantation. The study suggests that targeting glycolysis, a metabolic process, in these cells may be a potential treatment strategy. [Extracted from the article]

A study conducted by the University of Virginia School of Medicine has found that PANX1, a membrane channel involved in inflammation and blood pressure regulation, may play a role in heart failure. The researchers created a mouse model with PANX1 deletion in cardiomyocytes and found that this deletion increased glycolytic metabolism and protected against cardiac hypertrophy in nonischemic heart failure. Additionally, the study showed that PANX1 deficiency reduced immune cell recruitment to the myocardium. These findings suggest that inhibiting the PANX1 channel could be a potential therapeutic approach for treating heart failure. [Extracted from the article]

A recent study conducted at the Mayo Clinic in Rochester, Minnesota, has provided new insights into liver fibrosis. The researchers found that liver fibrosis is characterized by the activation of hepatic stellate cells (HSCs) and the release of fibrogenic extracellular vesicles (EVs), which are small particles involved in cell communication. The study demonstrated that inhibiting glycolysis, a metabolic process, in HSCs reduced liver fibrosis. Additionally, the researchers discovered that glycolysis in HSCs up-regulated the expression of genes related to EVs, which increased fibrotic gene expression in recipient HSCs. These findings suggest that targeting glycolysis in HSCs could be a potential therapeutic approach for liver fibrosis. [Extracted from the article]

A report from Nanchang University in Jiangxi, China discusses research on the role of CD52 in non-small cell lung cancer (NSCLC). The study found that CD52 expression was elevated in NSCLC and correlated with patient prognosis. Downregulation of CD52 suppressed the proliferation, migration, aerobic glycolysis, and tumorigenesis of NSCLC cells. The study concluded that CD52 knockdown inhibited aerobic glycolysis and malignant behavior of NSCLC cells through the AKT signaling pathway, suggesting it could be a potential therapeutic target for NSCLC. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of lactate dehydrogenase (LDH) in regulating glycolysis, the tricarboxylic acid cycle (TCAC), and oxidative phosphorylation (OXPHOS) in cancer cells. The study found that individual LDH A or B knockouts had minimal impact on these processes, but combining LDH knockout with LDH inhibitor GNE-140 significantly suppressed them. Inhibition of LDH disrupted glycolysis, leading to impaired TCAC and mitochondrial respiration. Under hypoxia, LDH inhibition had a stronger effect, inducing energy crisis, redox imbalance, and cancer cell death. The study highlights the intricate control of LDH over metabolic pathways and the interplay of enzyme kinetics and thermodynamics in metabolic regulation. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent research report from Sapporo Medical University in Japan explores the role of Rho-associated coiled-coil-containing protein kinase (ROCK) 2 in human trabecular meshwork (HTM) cells. The study found that a specific ROCK2 inhibitor, KD025, significantly suppressed glycolytic ATP production rate and increased mitochondrial ATP production rate in HTM cells. RNA sequencing analysis revealed differentially expressed genes (DEGs) related to cellular components and molecular functions, and Ingenuity Pathway Analysis (IPA) identified IL-6, STAT3, CSTA, and S1PR3 as possible regulators. The findings suggest that ROCK2 mediates signaling pathways related to basic biological activities such as glycolysis in HTM cells. [Extracted from the article]

A recent report from Columbia University Irving Medical Center discusses new research on cancer. The study focuses on the development of cell-penetrating peptides that target specific transcription factors and promote the death of cancer cells. The researchers found that one of these peptides, called Dpep, inhibits glucose uptake and glycolysis in certain cancer cell lines by upregulating the tumor suppressor TXNIP. The study also explores the potential of combining Dpep with other drugs for cancer treatment. Overall, the findings suggest that Dpep has the potential to induce apoptotic death in a range of cancer cells by suppressing glucose metabolism. [Extracted from the article]

A study conducted by researchers at Zhejiang University in China explores the role of Hepatitis B virus (HBV) in hepatocellular carcinoma (HCC), a leading cause of cancer-related mortality worldwide. The study focuses on the impact of HBV on glucose metabolism and investigates the involvement of a specific long non-coding RNA (lncRNA) called OIP5-AS1. The research findings suggest that HBV protein X (HBx) inhibits the expression of OIP5-AS1, which in turn suppresses the glycolysis process mediated by Hexokinase domain component 1 (HKDC1). The study concludes that OIP5-AS1 could serve as a diagnostic marker and therapeutic target for HBV-positive HCC patients. [Extracted from the article]

According to a preprint abstract from biorxiv.org, researchers have discovered a new role for endothelial Drp1 in promoting angiogenesis, the formation of new blood vessels. The study found that Drp1 acts as a redox sensor, transmitting signals from the growth factor VEGF to enhance glycolysis and angiogenesis. The researchers also observed impaired angiogenesis in mice with Drp1 deficiency or mutations that prevent cysteine oxidation. These findings provide new insights into the connections between redox signaling, glycolysis, and angiogenesis. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

Researchers at the Laboratory of Clinical in Pavia, Italy, have conducted a study on the toxic effects of methylglyoxal (MGO), a reactive byproduct of glycolysis and a potent glycating agent, on 3D human stem-cell-derived neuronal spheroids. The study found that MGO at concentrations comparable to those found in MGO-associated diseases caused cytotoxic effects, reduced cell growth and viability, and altered key signaling endpoints relevant to neurodegenerative diseases and aging. The use of 3D neuronal spheroids of human origin was shown to be a useful in vitro strategy for testing MGO and other dicarbonyls. The research was supported by the Ministero Della Salute. [Extracted from the article]

A study conducted by researchers at Shantou University in Guangdong, China, explored the role of MRTO4 in hepatocellular carcinoma (HCC). The study found that MRTO4 is an independent prognostic risk factor for HCC and accelerates the progression of the disease by promoting glycolysis and inhibiting ALDOB. The researchers suggest that inhibiting MRTO4 could be a potential therapeutic strategy for HCC. The study utilized various molecular biology research methods and analyzed clinical data from The Cancer Genome Atlas (TCGA). [Extracted from the article]

Researchers from Shandong Provincial Hospital in China have conducted a study on the regulatory roles and clinical significance of glycolysis in tumor progression. They found that glycolysis, a form of metabolic reprogramming, plays a significant role in the growth, proliferation, invasion, and metastasis of tumor cells. The researchers also discovered that glycolytic enzymes and products can serve as biomarkers for early diagnosis and prognostic assessment of tumors. Additionally, they identified potential therapeutic targets for tumor treatment through the inhibition of glycolytic enzymes. This study provides valuable insights into the role of glycolysis in tumor development and highlights its potential as a target for therapeutic interventions. [Extracted from the article]

A recent preprint abstract discusses the role of glycolysis in mature red blood cells (RBCs) and its impact on transfusion outcomes. The study utilized a large sample size of human volunteers and mice to identify associations between glycolytic metabolites and donor age, sex, and genetic polymorphisms. The levels of ATP and hypoxanthine, as well as the genetic traits linked to them, were found to be associated with hemolysis in vitro and in vivo, suggesting their potential as markers to improve transfusion outcomes. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A new study conducted by researchers at the Affiliated Hospital of Nantong University in China explores the role of glycolysis in cancer progression and its potential as a therapeutic target. The study reveals that tumor cells use glycolysis to obtain energy and macromolecules for multiplication, even in the presence of sufficient oxygen. The researchers also highlight the metabolic reprogramming of immune cells and stromal cells in the tumor microenvironment, which involves increased glycolysis. The review discusses potential targets and inhibitors of glycolysis and explores the viability of combining glycolysis inhibitors with immunotherapy and chemotherapy. Understanding the glycolytic processes in different cells within the tumor immunological milieu can inform the development of future treatment strategies. [Extracted from the article]

A study conducted at St. John's University in Queens, New York, focused on an MDM2 cancer-associated mutant variant called W329G. The researchers found that this mutant variant attenuates ribosomal stress-mediated p53 responses, promoting cell survival and glycolysis. The study suggests that the mutant cells are more resistant to cell growth inhibition induced by ribosomal stress and exhibit higher glycolytic rates. This research was supported by the National Institutes of Health (NIH) in the United States and has been peer-reviewed. [Extracted from the article]

Researchers from Hubei University in Wuhan, China have developed a nanocomposite material called Ca-CN/MnS that shows promise in treating methicillin-resistant Staphylococcus aureus (MRSA) infections in wounds. The nanocomposite, which combines Ca-doped g-C3N4 and MnS, exhibits efficient charge separation and can be activated by near-infrared light to produce reactive oxygen species and heat, resulting in a high bactericidal efficiency of 99.98%. Additionally, the introduction of biologically functional elements in the nanocomposite promotes wound healing by triggering the glycolysis and calcium signaling pathway. This research offers a potential solution for treating multidrug-resistant bacterial infections and accelerating tissue repair. [Extracted from the article]

A recent study conducted by researchers at the Shanghai University of Traditional Chinese Medicine has explored the issue of resistance to Poly (ADP-ribose) polymerase inhibitors (PARPi) in ovarian cancer treatment. The study found a correlation between PARPi resistance, glycolysis, and tumor angiogenesis in ovarian cancer. The researchers discovered that Paris saponin VII (PS VII), a natural compound, partially reversed PARPi resistance and showed synergistic effects when combined with PARPi. PS VII was found to hinder glycolysis and angiogenesis in PARPi-resistant ovarian cancer cells by binding and stabilizing the expression of ROR alpha, thus inhibiting ECM1 and interfering with the VEGFR2/FAK/AKT/GSK3 beta signaling pathway. This research provides new targeted treatment options for ovarian cancer and expands the application of PARPi in clinical treatment. [Extracted from the article]

A recent study conducted at Xiangya Hospital in Changsha, People's Republic of China, has found that xanthohumol, a natural compound, can inhibit the growth and glycolysis of ovarian cancer cells. The researchers discovered that xanthohumol promotes the degradation of S-phase kinase-associated protein 2 (Skp2), which is essential for the growth of ovarian cancer cells. This degradation leads to the suppression of the Skp2/AKT/HK2 signal pathway, ultimately inhibiting tumorigenesis. The study suggests that xanthohumol may have potential as an antitumor treatment for ovarian cancer. [Extracted from the article]

A new report from researchers at the First Affiliated Hospital with Nanjing Medical University discusses the use of minimally invasive thermal therapy as an alternative treatment to surgery for solid tumors. While this therapy has high complete ablation rates, tumor recurrence remains a concern. The researchers found that glycolysis inhibition, combined with microwave ablation therapy, enhances the differentiation of tumor-specific CD8+ TCM cells, leading to a long-term anti-tumor effect. This research offers a potential strategy to prevent tumor recurrence and provides a proof-of-principle for future clinical trials. [Extracted from the article]

A recent study conducted by researchers at Guangxi Medical University in China explores the potential of naringenin, a natural compound, in enhancing the effectiveness of ferroptosis inducers for the treatment of liver cancer. Ferroptosis is a type of programmed cell death induced by lipid peroxidation. The study found that the combination of naringenin and ferroptosis inducers resulted in more robust lipid peroxidation and severe damage to cancer cells compared to either treatment alone. The researchers also identified that the AMPK-PGC1a signaling axis plays a key role in naringenin's effect on reducing ferroptosis resistance in liver cancer. These findings suggest that naringenin could potentially improve cancer cell sensitivity to ferroptosis inducers, offering a promising therapeutic strategy for liver cancer treatment. [Extracted from the article]

According to a preprint abstract, researchers have found that the migration ability of natural killer (NK) cells, which are important for immune defense against HIV infection, is significantly impaired in HIV-infected individuals. The impairment of glycolysis, a metabolic process, was identified as the cause of this decreased migration. The study also revealed that the inhibitory receptor TIGIT plays a role in weakening the glycolysis of NK cells in HIV-infected individuals. This research provides new insights for potential immunotherapy in HIV infection. Please note that this preprint has not yet undergone peer review. [Extracted from the article]

A study conducted by researchers from Kumamoto University in Japan explores the impact of glycolytic enzymes on the replication of Human Immunodeficiency Virus Type 1 (HIV-1). The researchers found that HIV-1 infection changes cellular metabolism to aerobic glycolysis, which allows the virus to efficiently replicate even in this environment. The study discusses the regulatory role of glycolytic enzymes in viral replication and proposes a strategy to eliminate latently HIV-1-infected cells using the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH). The research provides insights into the cellular mechanisms involved in HIV/AIDS and potential strategies for antiviral treatment. [Extracted from the article]

A report from the University of Jinan in Guangdong, China discusses research on non-small cell lung cancer (NSCLC). The study focuses on the role of a specific long noncoding RNA (lncRNA) called RAMP2 antisense RNA1 (RAMP2-AS1) in NSCLC. The researchers found that downregulation of RAMP2-AS1 in NSCLC tissues was associated with increased glycolysis and reduced cell apoptosis. They also discovered that the fat mass and obesity-associated protein (FTO) played a role in the regulation of RAMP2-AS1 and glycolysis. The study provides insights for the development of new therapeutic strategies for NSCLC. [Extracted from the article]

A recent study conducted by researchers at Nantong University explores the role of ECHDC2, an enzyme in the Enoyl-CoA hydratase/isomerase family, in gastric cancer (GC). The study found that low expression of ECHDC2 in GC is associated with poor prognosis. Overexpression of ECHDC2 inhibits aerobic glycolysis and the proliferation of GC cells. The study also discovered that ECHDC2 promotes the degradation of MCCC2 protein by binding with NEDD4. These findings suggest that ECHDC2 could be a potential therapeutic target for GC. [Extracted from the article]

A recent study conducted by researchers at the First Affiliated Hospital of University of Science and Technology China (USTC) has found that inhibiting the protein SHP2 can reduce inflammation and promote functional recovery in mice with spinal cord injuries. The study focused on the role of microglia, a type of cell in the central nervous system, in the secondary inflammatory response following spinal cord injury. The researchers discovered that inhibiting SHP2 expression in microglia led to a reduction in inflammation and improved locomotor function in the mice. These findings suggest that targeting SHP2 could be a potential treatment for inflammation-related diseases and spinal cord injuries. [Extracted from the article]

New research from the Affiliated Cancer Hospital of Zhengzhou University explores the role of ubiquitin carboxyl terminal hydrolase L5 (UCHL5) in hepatocellular carcinoma (HCC), a highly malignant form of liver cancer. The study found that UCHL5 is strongly expressed in HCC and is associated with a worse prognosis for patients. UCHL5 promotes glycolysis, a metabolic process, in HCC cells by activating the Wnt/b-catenin pathway, leading to increased proliferation and metastasis of cancer cells. The findings suggest that UCHL5 could serve as a potential prognostic marker and therapeutic target for HCC treatment. [Extracted from the article]

Researchers from Guangxi Medical University in China have conducted a study on non-small cell lung cancer (NSCLC) and its response to oridonin (ORI), a component of the Chinese herb Herba Rabdosiae. The study found that ORI can inhibit the growth of NSCLC tumors by targeting key proteins involved in glycolysis, such as Aldolase A (ALDOA) and Enolase 1 (ENO1). This novel antitumor strategy of inhibiting glycolysis shows promise in suppressing NSCLC and triggering apoptosis. The research has been peer-reviewed and provides valuable insights into potential treatments for NSCLC. [Extracted from the article]

A recent study conducted by researchers at Guangxi Medical University in China has found that long non-coding RNAs (lncRNAs) play a significant role in the regulation of aerobic glycolysis in hepatocellular carcinoma (HCC), a type of liver cancer. The researchers discovered that lncRNAs can affect metabolic enzymes and signaling pathways, thereby influencing the occurrence and progression of HCC. The study suggests that lncRNAs could be potential therapeutic targets for antitumor cell metabolism. This research has been peer-reviewed and provides valuable insights into the understanding and treatment of liver cancer. [Extracted from the article]

Researchers at Hebei University of Chinese Medicine in Wuhan, China have conducted a study on the effects of lymphocyte antigen 6-complex K (LY6K) on the proliferation and energy metabolism of lung adenocarcinoma cells. The study found that high levels of LY6K expression in lung adenocarcinoma are associated with a poor prognosis. LY6K was found to promote cell proliferation and energy metabolism in A549 cells by regulating aerobic glycolysis. The research suggests that LY6K may play a role in the development and progression of lung cancer. [Extracted from the article]

A recent report from King's College London explores the relationship between glycolysis and breast cancer. The researchers hypothesize that the increased glycolytic flux in cancer cells is due to the ATP demand of Na+/K+-ATPase (NKA) caused by altered sodium ion homeostasis. Through experiments on human and murine breast cancer cells, the researchers found that inhibiting NKA resulted in elevated intracellular sodium levels and inhibited glycolytic flux in human cancer cells but not in murine cells. These findings suggest a correlation between glycolytic flux and NKA activity in breast cancer cells, providing insight into the mechanistic basis of the Warburg effect. [Extracted from the article]

A recent study conducted at the Third Affiliated Hospital focused on hepatocellular carcinoma (HCC), the most common form of liver cancer. The researchers aimed to understand the molecular mechanisms involved in HCC and find potential therapeutic strategies. They found that TNFa-stimulated gene-6 (TNFAIP6) plays a critical role in HCC and is associated with poor clinical prognosis. The study revealed that TNFAIP6 promotes aerobic glycolysis, a process that contributes to the malignancy of HCC. These findings provide insights into the development of clinical therapies for managing HCC. [Extracted from the article]

A recent study conducted by Fudan University in Shanghai, China, has found that lysine methyltransferase 5C (KMT5C) plays a role in the proliferation and metastasis of clear cell renal cell carcinoma (ccRCC) through aerobic glycolysis. The researchers discovered that KMT5C expression was significantly increased in ccRCC tissues and was closely associated with the overall survival rate of patients. By regulating glycolytic genes and EMT transcriptional factors, KMT5C promoted the growth and epithelial-mesenchymal transition of ccRCC cells. These findings suggest that KMT5C may serve as an oncoprotein and provide insights for molecular diagnosis and potential therapeutic strategies for ccRCC patients. [Extracted from the article]

A new study from Henan University of Science and Technology in China explores the effects of combining L-arginine and 5-fluorouracil (5-FU) on liver cancer cells. The researchers found that the combination resulted in decreased cell survival and synergistic cytotoxic effects. It also inhibited glucose metabolism and downregulated nuclear transcription factors, impeding the proliferation of hepatocellular carcinoma cells. The study suggests that the combination of L-arginine and 5-FU could be a potential treatment for liver cancer. [Extracted from the article]

A recent study conducted by researchers at Shanghai Jiao Tong University School of Medicine explores the role of growth differentiation factor 15 (GDF15) in sepsis-induced lung injury. The study found that GDF15 levels were correlated with various clinical markers of sepsis severity. In mouse models, recombinant GDF15 was shown to inhibit inflammation and reduce lung tissue injury. The researchers also discovered that GDF15 inhibits glycolysis and signaling pathways associated with inflammation. These findings provide new insights into potential therapeutic strategies for treating sepsis. [Extracted from the article]

A study conducted by the State Key Laboratory of Genetic Engineering explores the role of indoleamine 2,3-dioxygenase 1 (IDO1) in pancreatic cancer. The researchers found that IDO1, an enzyme involved in the breakdown of the essential amino acid tryptophan, affects glucose and lipid metabolism in addition to its known role in immune tolerance. The study reveals that IDO1 modulates glycolysis and glucose uptake in pancreatic cancer cells, and its inhibition can inhibit glycolysis, promote apoptosis, and potentially serve as a therapeutic strategy for pancreatic cancer. The research provides new insights into the understanding and treatment of pancreatic cancer. [Extracted from the article]