Altered metabolism in cancer: insights into energy pathways and therapeutic targets

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Сен. 18, 2024

Язык: Английский

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Metabolic reprogramming and therapeutic resistance in primary and metastatic breast cancer

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Ноя. 21, 2024

Metabolic alterations, a hallmark of cancer, enable tumor cells to adapt their environment by modulating glucose, lipid, and amino acid metabolism, which fuels rapid growth contributes treatment resistance. In primary breast metabolic shifts such as the Warburg effect enhanced lipid synthesis are closely linked chemotherapy failure. Similarly, metastatic lesions often display distinct profiles that not only sustain but also confer resistance targeted therapies immunotherapies. The review emphasizes two major aspects: mechanisms driving in both how unique environments sites further complicate treatment. By targeting vulnerabilities at stages, new strategies could improve efficacy existing provide better outcomes for cancer patients.

Язык: Английский

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Targeting KRAS: from metabolic regulation to cancer treatment

Molecular Cancer, Год журнала: 2025, Номер 24(1)

Опубликована: Янв. 11, 2025

The Kirsten rat sarcoma viral oncogene homolog (KRAS) protein plays a key pathogenic role in oncogenesis, cancer progression, and metastasis. Numerous studies have explored the of metabolic alterations KRAS-driven cancers, providing scientific rationale for targeting metabolism treatment. development KRAS-specific inhibitors has also garnered considerable attention, partly due to challenge acquired treatment resistance. Here, we review reprogramming glucose, glutamine, lipids regulated by oncogenic KRAS, with an emphasis on recent insights into relationship between changes mechanisms driven KRAS mutant related advances targeted therapy. We focus inhibitor discovery strategies colorectal, pancreatic, non-small cell lung cancer, including current clinical trials. Therefore, this provides overview understanding associated mutation therapeutic strategies, aiming facilitate challenges support investigation strategies.

Язык: Английский

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Glutamine and cancer: metabolism, immune microenvironment, and therapeutic targets

Cell Communication and Signaling, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 24, 2025

Язык: Английский

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Targeting the glutamine-arginine-proline metabolism axis in cancer

Journal of Enzyme Inhibition and Medicinal Chemistry, Год журнала: 2024, Номер 39(1)

Опубликована: Июль 25, 2024

Metabolic abnormalities are an important feature of tumours. The glutamine-arginine-proline axis is node cancer metabolism and plays a major role in amino acid metabolism. This also acts as scaffold for the synthesis other nonessential acids essential metabolites. In this paper, we briefly review (1) glutamine addiction exhibited by tumour cells with accelerated transport metabolism; (2) methods regulating extracellular entry, intracellular fate glutamine; (3) glutamine, proline arginine metabolic pathways their interaction; (4) research progress therapy targeting system, focus on summarising therapeutic strategies one key enzymes P5CS (ALDH18A1). provides new basis treatments characteristics

Язык: Английский

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The molecular code of kidney cancer: A path of discovery for gene mutation and precision therapy

Molecular Aspects of Medicine, Год журнала: 2025, Номер 101, С. 101335 - 101335

Опубликована: Янв. 1, 2025

Renal cell carcinoma (RCC) is a malignant tumor with highly heterogeneous and complex molecular mechanisms. Through systematic analysis of TCGA, COSMIC other databases, 24 mutated genes closely related to RCC were screened, including VHL, PBRM1, BAP1 SETD2, which play key roles in signaling pathway transduction, chromatin remodeling DNA repair. The PI3K/AKT/mTOR particularly important the pathogenesis RCC. Mutations such as PIK3CA, MTOR PTEN are associated metabolic abnormalities proliferation. Clinically, mTOR inhibitors VEGF-targeted drugs have shown significant efficacy personalized therapy. Abnormal regulation reprogramming, especially glycolysis glutamine pathways, provides cells continuous energy supply survival advantages, GLS1 promising results preclinical studies. This paper also explores potential immune checkpoint combination targeted drugs, well application nanotechnology drug delivery In addition, unique mechanisms revealed individualized therapeutic strategies explored for specific subtypes TFE3, TFEB rearrangement type SDHB mutant type. review summarizes common gene mutations their mechanisms, emphasizes diagnosis, treatment prognosis, looks forward prospects multi-pathway therapy, immunotherapy treatment, providing theoretical support clinical guidance new development.

Язык: Английский

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Glutamine Supplementation as an Anticancer Strategy: A Potential Therapeutic Alternative to the Convention

Cancers, Год журнала: 2024, Номер 16(5), С. 1057 - 1057

Опубликована: Март 5, 2024

Glutamine, a multifaceted nonessential/conditionally essential amino acid integral to cellular metabolism and immune function, holds pivotal importance in the landscape of cancer therapy. This review delves into intricate dynamics surrounding both glutamine antagonism strategies supplementation within context treatment, emphasizing critical role progression Glutamine antagonism, aiming disrupt tumor growth by targeting metabolic pathways, is challenged adaptive nature cells complex microenvironment, potentially compromising its therapeutic efficacy. In contrast, supports improves gut integrity, alleviates treatment-related toxicities, patient well-being. Moreover, recent studies highlighted contributions epigenetic regulation potential bolster anti-cancer functions. However, implementation necessitates careful consideration interactions with ongoing treatment regimens delicate equilibrium between supporting normal function promoting tumorigenesis. By critically assessing implications supplementation, this aims offer comprehensive insights for effective management.

Язык: Английский

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Targeting Metabolic–Redox Nexus to Regulate Drug Resistance: From Mechanism to Tumor Therapy

Antioxidants, Год журнала: 2024, Номер 13(7), С. 828 - 828

Опубликована: Июль 10, 2024

Drug resistance is currently one of the biggest challenges in cancer treatment. With deepening understanding drug resistance, various mechanisms have been revealed, including metabolic reprogramming and alterations redox balance. Notably, mediates survival tumor cells harsh environments, thereby promoting development resistance. In addition, changes during pattern shift trigger reactive oxygen species (ROS) production, which turn regulates cellular metabolism, DNA repair, cell death, metabolism direct or indirect ways to influence sensitivity tumors therapies. Therefore, intersection ROS profoundly affects clarifying entangled may be beneficial for developing drugs treatment methods thwart this review, we will summarize regulatory mechanism on highlight recent therapeutic strategies targeting metabolic-redox circuits, dietary interventions, novel chemosynthetic drugs, combination regimens, delivery systems.

Язык: Английский

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Metabolic Reprogramming at the Edge of Redox: Connections Between Metabolic Reprogramming and Cancer Redox State

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(2), С. 498 - 498

Опубликована: Янв. 9, 2025

The importance of redox systems as fundamental elements in biology is now widely recognized across diverse fields, from ecology to cellular biology. Their connection metabolism particularly significant, it plays a critical role energy regulation and distribution within organisms. Over recent decades, has emerged relevant focus studies biological regulation, especially following its recognition hallmark cancer. This shift broadened cancer research beyond strictly genetic perspectives. interaction between carcinogenesis involves the essential metabolic pathways, such glycolysis Krebs cycle, well involvement redox-active components like specific amino acids cofactors. feedback mechanisms linking highlight development patterns that enhance flexibility adaptability tumor processes, influencing larger-scale phenomena circadian rhythms epigenetics.

Язык: Английский

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Deciphering the Controversial Role of TP53 Inducible Glycolysis and Apoptosis Regulator (TIGAR) in Cancer Metabolism as a Potential Therapeutic Strategy

Cells, Год журнала: 2025, Номер 14(8), С. 598 - 598

Опубликована: Апрель 15, 2025

Tumor metabolism has emerged as a critical target in cancer therapy, revolutionizing our understanding of how cells grow, survive, and respond to treatment. Historically, research focused on genetic mutations driving tumorigenesis, but recent decades, metabolic reprogramming been recognized hallmark cancer. The TP53 inducible glycolysis apoptosis regulator, or TIGAR, affects wide range cellular molecular processes plays key role cell by regulating the balance between antioxidant defense mechanisms. Cancer often exhibit shift towards aerobic (the Warburg effect), which allows rapid energy production gives rise biosynthetic intermediates for proliferation. By inhibiting glycolysis, TIGAR can reduce proliferation rate cells, particularly early-stage tumors specific tissue types. This may limit resources available division, thereby exerting tumor-suppressive effect. However, this also leads increased levels reactive oxygen species (ROS), damage if not properly managed. helps protect from excessive ROS promoting pentose phosphate pathway (PPP), generates NADPH—a molecule involved defense. Through its actions, decreases glycolytic flux while increasing diversion glucose-6-phosphate into PPP. reduces supports biosynthesis survival maintaining nucleotides lipids. emerging prognostic potential therapeutic different types cancers. review highlights cancer, evaluating diagnostic marker target.

Язык: Английский

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