Catabolic cancer-associated fibroblasts transfer energy and biomass to anabolic cancer cells, fueling tumor growth

Martinez‐Outschoorn, Ubaldo; Lisanti, Michael P.; Sotgia, Federica

doi:10.1016/j.semcancer.2014.01.005

Cited by 349 publications

(386 citation statements)

References 218 publications

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“…Orimo et al [27] showed that CAF from primary human breast cancers significantly enhanced tumor growth and angiogenesis in xenograft models. Recently, a metabolic partnership between catabolic fibroblasts and anabolic cancer cells with creation of a nutrition-rich environment has been proposed [28]. …”

Section: Components Of the Microenvironment And Their Interplay With mentioning

confidence: 99%

Role of the Tumor Microenvironment in Breast Cancer

Soysal

Tzankov²,

Muenst³

2015

Pathobiology

377

261

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In recent years, it has been shown that breast cancer consists not only of neoplastic cells, but also of significant alterations in the surrounding stroma or tumor microenvironment. These alterations are now recognized as a critical element for breast cancer development and progression, as well as potential therapeutic targets. Various components of the breast cancer microenvironment, such as suppressive immune cells, soluble factors and altered extracellular matrix, act together to impede effective antitumor immunity and promote breast cancer progression and metastasis. Stromal cells in the breast cancer microenvironment are characterized by molecular alterations and aberrant signaling pathways, some of which are prognostic of clinical outcome. Several new therapies targeting stromal components are in development or undergoing clinical trials. We focus herein on the composition of the breast cancer microenvironment and concomitant molecular alterations, the specific interplay between various cell types and cancer cells, and the clinical implications of these findings.

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Section: Components Of the Microenvironment And Their Interplay With mentioning

confidence: 99%

Role of the Tumor Microenvironment in Breast Cancer

Soysal

Tzankov²,

Muenst³

2015

Pathobiology

377

261

View full text Add to dashboard Cite

show abstract

“…Subsequently, CAFs secrete energy-rich metabolites, such as ketone bodies, lactate, and pyruvate, which in turn can be taken up by cancer cells and oxidized in the mitochondria for energy production (62). Accumulating evidence suggests that glycolytic CAFs promote tumor progression (63). Given the major role of CAFs in tumor progression, the Reverse Warburg effect may represent an important metabolic hallmark of CAFs.…”

Section: The Reverse Warburg Effectmentioning

confidence: 99%

“…As with metabolic interactions between distinct tumor subpopulations, metabolic coupling between CAFs and cancer cells relies upon unique MCT expression patterns within these compartments. Epithelial cancer cells typically express high level of MCT1, thus promoting the uptake of lactate from the MCT4-expressing CAFs (63,66). Interestingly, metabolic coupling between cancer cells and stromal cells may occur in an opposite fashion.…”

Section: The Reverse Warburg Effectmentioning

confidence: 99%

Metabolic Plasticity as a Determinant of Tumor Growth and Metastasis

et al. 2016

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Cancer cells must adapt their metabolism to meet the energetic and biosynthetic demands that accompany rapid growth of the primary tumor and colonization of distinct metastatic sites. Different stages of the metastatic cascade can also present distinct metabolic challenges to disseminating cancer cells. However, little is known regarding how changes in cellular metabolism, both within the cancer cell and the metastatic microenvironment, alter the ability of tumor cells to colonize and grow in distinct secondary sites. This review examines the concept of metabolic heterogeneity within the primary tumor, and how cancer cells are metabolically coupled with other cancer cells that comprise the tumor and cells within the tumor stroma. We examine how metabolic strategies, which are engaged by cancer cells in the primary site, change during the metastatic process. Finally, we discuss the metabolic adaptations that occur as cancer cells colonize foreign metastatic microenvironments and how cancer cells influence the metabolism of stromal cells at sites of metastasis. Through a discussion of these topics, it is clear that plasticity in tumor metabolic programs, which allows cancer cells to adapt and grow in hostile microenvironments, is emerging as an important variable that may change clinical approaches to managing metastatic disease. Cancer Res; 76(18); 5201-8. Ó2016 AACR.

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“…Recent studies have described metabolic coupling among stromal cells such as cancer-associated ibroblasts (CAFs), adipocytes, immune cells, and neoplastic cells [82][83][84][85][86][87][88][89][90]. Glycolytic CAFs can provide nutrients such as lactates and ketones as fuel for tumor cells [82][83][84]. Adipocytes produce free faty acids and promote faty acid oxidation in tumor cells [85].…”

Section: Glycolysis In Osteosarcomamentioning

confidence: 99%

Microenvironment Signals and Mechanisms in the Regulation of Osteosarcoma

Mai¹,

Zhang²,

Xie³

et al. 2017

Osteosarcoma - Biology, Behavior and Mechanisms

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Osteosarcoma (OS) is the most common malignant primary bone tumor in children and adolescents and features rapid development, strong metastatic ability, and poor prognosis. It has been well established that diverse genetic aberrations and metabolic alterations confer the tumorigenesis and development of OS. The intricate metabolism and vascularization that contributes to the nutrient and structural support for tumor progression should be thoroughly clariied to help us gain novel insights into OS and its clinical diagnoses and treatments. With regard to the complex bone extracellular matrix (ECM) and local cell populations, we intend to illustrate the interrelationship between various microenvironmental signals and the diferent stages of OS evolution. Solid evidence has noted two crucial factors of the OS microenvironment in the acquisition of stem cell phenotypes -transforming growth factor-β1 (TGF-β1) signaling and hypoxia. Diferent cell subtypes in the local environment might also serve as unique contributors that interact with each other and communicate with distant cells, thus participating in local invasion and metastasis. Proper models have been established and improved to reveal the evolutionary footsteps of how normal cells transform into a neoplastic state and progress toward malignancy.

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Catabolic cancer-associated fibroblasts transfer energy and biomass to anabolic cancer cells, fueling tumor growth

Cited by 349 publications

References 218 publications

Role of the Tumor Microenvironment in Breast Cancer

Role of the Tumor Microenvironment in Breast Cancer

Metabolic Plasticity as a Determinant of Tumor Growth and Metastasis

Microenvironment Signals and Mechanisms in the Regulation of Osteosarcoma

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