Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: April 9, 2025
Language: Английский
Nature Cancer, Journal Year: 2024, Volume and Issue: 5(3), P. 384 - 399
Published: March 22, 2024
Language: Английский
Citations
57
Nature reviews. Cancer, Journal Year: 2024, Volume and Issue: 24(5), P. 316 - 337
Published: April 16, 2024
Language: Английский
Citations
26
Clinical and Translational Medicine, Journal Year: 2024, Volume and Issue: 14(3)
Published: March 1, 2024
Abstract Heightened lactate production in cancer cells has been linked to various cellular mechanisms such as angiogenesis, hypoxia, macrophage polarisation and T‐cell dysfunction. The lactate‐induced lactylation of histone lysine residues is noteworthy, it functions an epigenetic modification that directly augments gene transcription from chromatin. This originating effectively fosters a reliance on transcription, thereby expediting tumour progression development. Herein, this review explores the correlation between characteristics, revealing innovative process enhances vulnerability malignancy. Moreover, imperative acknowledge paramount importance acknowledging therapeutic methodologies for proficiently managing by precisely targeting signalling. comprehensive illuminates crucial yet inadequately investigated aspect lactylation, providing valuable insights into its clinical ramifications prospective interventions centred lactylation.
Language: Английский
Citations
17
Small, Journal Year: 2024, Volume and Issue: 20(29)
Published: March 3, 2024
Triple negative breast cancer (TNBC) cells have a high demand for oxygen and glucose to fuel their growth spread, shaping the tumor microenvironment (TME) that can lead weakened immune system by hypoxia increased risk of metastasis. To disrupt this vicious circle improve therapeutic efficacy, strategy is proposed with synergy ferroptosis, immunosuppression reversal disulfidptosis. An intelligent nanomedicine GOx-IA@HMON@IO successfully developed realize strategy. The Fe release behaviors indicate glutathione (GSH)-responsive degradation HMON. results titanium sulfate assay, electron spin resonance (ESR) spectra, 5,5'-Dithiobis-(2-nitrobenzoic acid (DTNB) assay T
Language: Английский
Citations
16
Molecular Cancer, Journal Year: 2025, Volume and Issue: 24(1)
Published: Jan. 13, 2025
Abstract KRAS is one of the most mutated genes, driving alternations in metabolic pathways that include enhanced nutrient uptaking, increased glycolysis, elevated glutaminolysis, and heightened synthesis fatty acids nucleotides. However, beyond mechanisms KRAS-modulated cancer metabolisms remain incompletely understood. In this review, we aim to summarize current knowledge on KRAS-related alterations cells explore prevalence significance mutation shaping tumor microenvironment influencing epigenetic modification via various molecular activities. Given rely these changes sustain cell growth survival, targeting processes may represent a promising therapeutic strategy for KRAS-driven cancers.
Language: Английский
Citations
4
Cell Reports Medicine, Journal Year: 2025, Volume and Issue: unknown, P. 101928 - 101928
Published: Jan. 1, 2025
Pancreatic ductal adenocarcinoma (PDAC) relies heavily on glutamine (Gln) utilization to meet its metabolic and biosynthetic needs. How epigenetic regulators contribute the flexibility PDAC's response adaptation Gln scarcity in tumor milieu remains largely unknown. Here, we elucidate that prolonged restriction or treatment with antagonist, 6-diazo-5-oxo-L-norleucine (DON), leads growth inhibition ferroptosis program activation PDAC. A CRISPR-Cas9 screen identifies an regulator, Paxip1, which promotes H3K4me3 upregulation Hmox1 transcription upon DON treatment. Additionally, ferroptosis-related repressors (e.g., Slc7a11 Gpx4) are increased as adaptive response, thereby predisposing PDAC cells deprivation. Moreover, sensitizes GPX4 inhibitor-induced ferroptosis, both vitro patient-derived xenografts (PDXs). Taken together, our findings reveal targeting dependency confers susceptibility GPX4-dependent via remodeling provides a combination strategy for therapy.
Language: Английский
Citations
2
Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)
Published: Feb. 2, 2025
Protein O-GlcNAcylation is a post-translational modification coupled to cellular metabolic plasticity. Aberrant has been observed in many cancers including endometrial cancer (EC), common malignancy women. However, clinical characterization of dysregulated homeostasis EC and interrogating its molecular mechanism remain incomplete. Here we report that level positively correlated with histologic grade Chinese cohort containing 219 tumors, validated The Cancer Genome Atlas dataset. Increasing patient-derived epithelial organoids promotes proliferation stem-like cell properties, whereas decreasing limits the growth organoids. CRISPR screen biochemical reveal tumor suppressor F-box only protein 31 (FBXO31) regulates by ubiquitinating O-GlcNAc transferase OGT. Downregulation impedes formation mouse models. Collectively, our study highlights as useful stratification marker therapeutic vulnerability for advanced, poorly differentiated cases. linked (EC). authors grade, FBXO31
Language: Английский
Citations
2
Trends in Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(6), P. 592 - 604
Published: April 10, 2024
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive form of pancreatic cancer, known for its challenging diagnosis and limited treatment options. The focus on metabolic reprogramming as key factor in tumor initiation, progression, therapy resistance has gained prominence. In this review we the impact changes interplay among stromal, immune, cells, glutamine branched-chain amino acids (BCAAs) emerge pivotal players modulating immune cell functions growth. We also discuss ongoing clinical trials that explore modulation PDAC, targeting mitochondrial metabolism, asparagine addiction, autophagy inhibition. Overcoming challenges understanding nutrient effects immune-stromal-tumor interactions holds promise innovative therapeutic strategies.
Language: Английский
Citations
14
Cancer Discovery, Journal Year: 2024, Volume and Issue: 14(6), P. 934 - 952
Published: March 29, 2024
Metastases, which are the leading cause of death in patients with cancer, have metabolic vulnerabilities. Alterations metabolism fuel energy and biosynthetic needs metastases but also needed to activate cell state switches cells invasion, migration, colonization, outgrowth distant organs. Specifically, metabolites can protein kinases as well receptors they crucial substrates for posttranslational modifications on histone nonhistone proteins. Moreover, enzymes moonlighting functions by acting catalytically, mainly kinases, or noncatalytically through protein-protein interactions. Here, we summarize current knowledge signaling cancer metastasis. Effective drugs prevention treatment will an immediate impact patient survival. To overcome lack such drugs, a better understanding molecular processes that Achilles heel metastasizing is needed. One emerging opportunity changes need undergo successfully metastasize grow Mechanistically, these not only fulfill biomass demands, often common between normal fast proliferating cells, enables particularly important cells.
Language: Английский
Citations
12
Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(8)
Published: Aug. 1, 2024
Abstract Pancreatic cancer is an aggressive with a poor prognosis. Metabolic abnormalities are one of the hallmarks pancreatic cancer, and cells can adapt to biosynthesis, energy intake, redox needs through metabolic reprogramming tolerate nutrient deficiency hypoxic microenvironments. use glucose, amino acids, lipids as maintain malignant growth. Moreover, they also metabolically interact in tumour microenvironment change cell fate, promote progression, even affect immune responses. Importantly, changes at body level deserve more attention. Basic research clinical trials based on targeted therapy or combination other treatments full swing. A comprehensive in-depth understanding regulation will not only enrich mechanisms disease progression but provide inspiration for new diagnostic therapeutic approaches.
Language: Английский
Citations
12