MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

Zheng, Yu-Kun; Zhou, Zhongshi; Wang, Guang-Zhong; Tu, Jiyuan; Cheng, Huan-Bo; Ma, Shang-zhi; Ke, Chang; Wang, Yan; Jian, Qi-Pan; Shu, Yu-Hang; Wu, Xiaowei

doi:10.1038/s41419-023-05761-9

Cited by 2 publications

(2 citation statements)

References 69 publications

(59 reference statements)

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“…USP18 expression poses an increased cellular FAO as a target to fatty acid metabolism in NSCLC [ 148 ]. Target hypoxic cancer cells with the combination of β-oxidation inhibitor etomoxir and radiation is proven for anti-lung adenocarcinoma [ 149 ]. Long-chain acyl-CoA dehydrogenase (ACADL) as an enzyme that regulates β-oxidation is a promising target for regulating Hippo/YAP pathway to confer anti-tumor imunity [ 136 ].…”

Section: Blocking Common Nsclc Metabolic Pathways As Anti-nsclcmentioning

confidence: 99%

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Bajinka,

Ouedraogo,

Golubnitschaja

et al. 2024

EPMA Journal

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Energy metabolism is a hub of governing all processes at cellular and organismal levels such as, on one hand, reparable vs. irreparable cell damage, cell fate (proliferation, survival, apoptosis, malignant transformation etc.), and, on the other hand, carcinogenesis, tumor development, progression and metastazing versus anti-cancer protection and cure. The orchestrator is the mitochondria who produce, store and invest energy, conduct intracellular and systemically relevant signals decisive for internal and environmental stress adaptation, and coordinate corresponding processes at cellular and organismal levels. Consequently, the quality of mitochondrial health and homeostasis is a reliable target for health risk assessment at the stage of reversible damage to the health followed by cost-effective personalized protection against health-to-disease transition as well as for targeted protection against the disease progression (secondary care of cancer patients against growing primary tumors and metastatic disease).The energy reprogramming of non-small cell lung cancer (NSCLC) attracts particular attention as clinically relevant and instrumental for the paradigm change from reactive medical services to predictive, preventive and personalized medicine (3PM). This article provides a detailed overview towards mechanisms and biological pathways involving metabolic reprogramming (MR) with respect to inhibiting the synthesis of biomolecules and blocking common NSCLC metabolic pathways as anti-NSCLC therapeutic strategies. For instance, mitophagy recycles macromolecules to yield mitochondrial substrates for energy homeostasis and nucleotide synthesis. Histone modification and DNA methylation can predict the onset of diseases, and plasma C7 analysis is an efficient medical service potentially resulting in an optimized healthcare economy in corresponding areas. The MEMP scoring provides the guidance for immunotherapy, prognostic assessment, and anti-cancer drug development. Metabolite sensing mechanisms of nutrients and their derivatives are potential MR-related therapy in NSCLC. Moreover, miR-495-3p reprogramming of sphingolipid rheostat by targeting Sphk1, 22/FOXM1 axis regulation, and A2 receptor antagonist are highly promising therapy strategies. TFEB as a biomarker in predicting immune checkpoint blockade and redox-related lncRNA prognostic signature (redox-LPS) are considered reliable predictive approaches.Finally, exemplified in this article metabolic phenotyping is instrumental for innovative population screening, health risk assessment, predictive multi-level diagnostics, targeted prevention, and treatment algorithms tailored to personalized patient profiles—all are essential pillars in the paradigm change from reactive medical services to 3PM approach in overall management of lung cancers. This article highlights the 3PM relevant innovation focused on energy metabolism as the hub to advance NSCLC management benefiting vulnerable subpopulations, affected patients, and healthcare at large.

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Section: Blocking Common Nsclc Metabolic Pathways As Anti-nsclcmentioning

confidence: 99%

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Bajinka,

Ouedraogo,

Golubnitschaja

et al. 2024

EPMA Journal

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“…Internal factors Oncogenic factor p53 regulates metabolism through its non-classical pathway and inhibits tumorigenesis. Wild-type p53 (wt p53) promotes FAO and inhibits tumor proliferation by up-regulating the expression of carnitine palmitoyltransferase 1C (CPT1C), malonyl coenzyme A decarboxylase (MCD), and lipoprotein 1 (LPIN1) ( Zhuang et al, 2019 ; Fadó et al, 2023 ; Mao and Jiang, 2023 ; Wang et al, 2023 ; Zheng et al, 2023 ). Mutant p53 reduces phosphorylation of acetyl coenzyme A carboxylase (ACC) by inhibiting AMP-activated protein kinase (AMPK), leading to increased malonyl coenzyme A levels and CPT1 receives inhibition, resulting in decreased FAO levels as well as enhancement of the lipid synthesis pathway ( Zhou et al, 2014 ; Herzig and Shaw, 2018 ).…”

Section: Targeting Lipid Metabolismmentioning

confidence: 99%

Mitochondrial inhibitors: a new horizon in breast cancer therapy

Yan,

Li,

et al. 2024

Front. Pharmacol.

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Breast cancer, due to resistance to standard therapies such as endocrine therapy, anti-HER2 therapy and chemotherapy, continues to pose a major health challenge. A growing body of research emphasizes the heterogeneity and plasticity of metabolism in breast cancer. Because differences in subtypes exhibit a bias toward metabolic pathways, targeting mitochondrial inhibitors shows great potential as stand-alone or adjuvant cancer therapies. Multiple therapeutic candidates are currently in various stages of preclinical studies and clinical openings. However, specific inhibitors have been shown to face multiple challenges (e.g., single metabolic therapies, mitochondrial structure and enzymes, etc.), and combining with standard therapies or targeting multiple metabolic pathways may be necessary. In this paper, we review the critical role of mitochondrial metabolic functions, including oxidative phosphorylation (OXPHOS), the tricarboxylic acid cycle, and fatty acid and amino acid metabolism, in metabolic reprogramming of breast cancer cells. In addition, we outline the impact of mitochondrial dysfunction on metabolic pathways in different subtypes of breast cancer and mitochondrial inhibitors targeting different metabolic pathways, aiming to provide additional ideas for the development of mitochondrial inhibitors and to improve the efficacy of existing therapies for breast cancer.

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MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer

Cited by 2 publications

References 69 publications

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Mitochondrial inhibitors: a new horizon in breast cancer therapy

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