The critical function of metabolic reprogramming in cancer metastasis

Xie, Sun‐Zhe; Pan, Junjie; Xu, Jianfeng; Zhu, Wenwei; Qin, Lun–Xiu

doi:10.1002/aac2.12044

Cited by 7 publications

(5 citation statements)

References 221 publications

(380 reference statements)

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“…CopyRight@ Susinjan Bhattacharya It is not only metabolic changes, but also epigenetic changes that help in the metabolic adaptation of the cancer cells in TME. Additionally, non-tumour cells in TME also undergo metabolic reprogramming [12]. The altered metabolic pathway sustains a pool of nutrients and energy for the cancer cells to grow.…”

Section: American Journal Of Biomedical Science and Researchmentioning

confidence: 99%

“…Diet can be an important component to reducing cancer aggressiveness and progression [6,11], but it is of high importance that diet as a therapeutic intervention must Am J Biomed Sci & Res progress along with the mode of primary treatment. Diet makes cells undergo metabolic programming in normal cells as well as reprogramming in cancer cells, wherein the latter is a hallmark of malignancy [12]. Dietary restriction also leads to metabolic reprogramming and can be thought of as a therapeutic approach as the process extends the lifespan of an organism and the process is linked to energy intake restriction without essential nutrient deficiency [13].…”

Section: Introductionmentioning

confidence: 99%

“…The tumour microenvironment (TME) involves the interaction of metabolic reprogramming with tumour cells and non-tumour cells, suggesting therapeutic strategies to target metabolic interventions [12]. With the growing incidences of cancer, it is necessary to investigate the metabolic reprogramming occurring in cancer cells and the possible dietary interventions along with the first-line therapy as medical care for cancer patients [16].…”

Section: Introductionmentioning

confidence: 99%

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Metabolic Reprogramming and Cancer: 2022

Bhattacharya¹

2023

AJBSR

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Cancer is a disease that is considered a silent killer. Early therapeutic interventions can lead to a cure for the disease. The causal reasons for cancer are many. At the molecular level, metabolic reprogramming is a process for self-renewal and survival by cancer cells. Dietary constituents are an important factor that leads to metabolic transitions and induces cellular reprogramming. The process is initiated by inducing changes in metabolism leading to the supply of nutrients and energy to the tumour cells, and this is linked to the induction of epithelial mesenchymal transition (EMT) and vascular mimicry (VM). Thermodynamic changes that get distinguished between proliferating and non-proliferating cells might also be a possible reason for cellular reprogramming. The entire process of metabolic reprogramming is linked to diet-driven changes and bioenergetics. The work here elucidates in brief the dependency of metabolic reprogramming on different factors, or stages and highlights possibilities for therapeutic interventions as part of cancer therapeutics.

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Section: American Journal Of Biomedical Science and Researchmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Metabolic Reprogramming and Cancer: 2022

Bhattacharya¹

2023

AJBSR

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“…Differentiated non-malignant cells and slowly proliferating tumour stem cells derive most of their ATP from OXPHOS. However, rapidly proliferating cells such as less differentiated cancer cells and activated immune cells generate most of their ATP through aerobic glycolysis ( 6 – 8 ).…”

Section: Introductionmentioning

confidence: 99%

Residual OXPHOS is required to drive primary and metastatic lung tumours in an orthotopic breast cancer model

Herst,

Carson,

Lewthwaite

et al. 2024

Front. Oncol.

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BackgroundFast adaptation of glycolytic and mitochondrial energy pathways to changes in the tumour microenvironment is a hallmark of cancer. Purely glycolytic ρ0 tumour cells do not form primary tumours unless they acquire healthy mitochondria from their micro-environment. Here we explored the effects of severely compromised respiration on the metastatic capability of 4T1 mouse breast cancer cells.Methods4T1 cell lines with different levels of respiratory capacity were generated; the Seahorse extracellular flux analyser was used to evaluate oxygen consumption rates, fluorescent confocal microscopy to assess the number of SYBR gold-stained mitochondrial DNA nucleoids, and the presence of the ATP5B protein in the cytoplasm and fluorescent in situ nuclear hybridization was used to establish ploidy. MinION nanopore RNA sequence analysis was used to compare mitochondrial DNA transcription between cell lines. Orthotopic injection was used to determine the ability of cells to metastasize to the lungs of female Balb/c mice.ResultsOXPHOS-deficient ATP5B-KO3.1 cells did not generate primary tumours. Severely OXPHOS compromised ρ0D5 cells generated both primary tumours and lung metastases. Cells generated from lung metastasis of both OXPHOS-competent and OXPHOS-compromised cells formed primary tumours but no metastases when re-injected into mice. OXPHOS-compromised cells significantly increased their mtDNA content, but this did not result in increased OXPHOS capacity, which was not due to decreased mtDNA transcription. Gene set enrichment analysis suggests that certain cells derived from lung metastases downregulate their epithelial-to-mesenchymal related pathways.ConclusionIn summary, OXPHOS is required for tumorigenesis in this orthotopic mouse breast cancer model but even very low levels of OXPHOS are sufficient to generate both primary tumours and lung metastases.

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“…Metastasis occurs when cancer cells divide and spread from the main tumor to other parts of the body via the circulatory or lymphatic systems ( 1 ). 90% of cancer-related fatalities are caused by metastasis ( 2 , 3 ). In particular, brain metastasis is a significant problem that often results in terrible effects for the patient ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

TME-targeted approaches of brain metastases and its clinical therapeutic evidence

Khan,

Sala

et al. 2023

Front. Immunol.

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The tumor microenvironment (TME), which includes both cellular and non-cellular elements, is now recognized as one of the major regulators of the development of primary tumors, the metastasis of which occurs to specific organs, and the response to therapy. Development of immunotherapy and targeted therapies have increased knowledge of cancer-related inflammation Since the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCB) limit immune cells from entering from the periphery, it has long been considered an immunological refuge. Thus, tumor cells that make their way “to the brain were believed to be protected from the body’s normal mechanisms of monitoring and eliminating them. In this process, the microenvironment and tumor cells at different stages interact and depend on each other to form the basis of the evolution of tumor brain metastases. This paper focuses on the pathogenesis, microenvironmental changes, and new treatment methods of different types of brain metastases. Through the systematic review and summary from macro to micro, the occurrence and development rules and key driving factors of the disease are revealed, and the clinical precision medicine of brain metastases is comprehensively promoted. Recent research has shed light on the potential of TME-targeted and potential treatments for treating Brain metastases, and we’ll use that knowledge to discuss the advantages and disadvantages of these approaches.

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The critical function of metabolic reprogramming in cancer metastasis

Cited by 7 publications

References 221 publications

Metabolic Reprogramming and Cancer: 2022

Metabolic Reprogramming and Cancer: 2022

Residual OXPHOS is required to drive primary and metastatic lung tumours in an orthotopic breast cancer model

TME-targeted approaches of brain metastases and its clinical therapeutic evidence

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