Glycolysis is the primary bioenergetic pathway for cell motility and cytoskeletal remodeling in human prostate and breast cancer cells

Shiraishi, Takeshi; Verdone, James E.; Huang, Jessie; Kahlert, Ulf D.; Hernandez, James R.; Torga, Gonzalo; Zarif, Jelani C.; Epstein, Tamir; Gatenby, Robert A.; McCartney, Annemarie M.; Elisseeff, Jennifer H.; Mooney, Steven M.; An, Steven S.; Pienta, Kenneth J.

doi:10.18632/oncotarget.2766

Cited by 156 publications

(147 citation statements)

References 44 publications

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“…A select few, likely those that undergo an epithelial-mesenchymal transition (EMT), will have the option to employ a mobile foraging strategy. Generally these cells have higher energy requirements and consume more resources than their stationary epithelial-like counterparts (33). Since very few cells in the primary tumor undergo EMT, the number of stationary foraging cells is likely to vastly outnumber mobile foraging cells.…”

Section: Optimal Foraging Of Prostate Cancermentioning

confidence: 99%

“…The genetic and molecular bases for cell movement behaviors and metastatic propensity in prostate cancer have been extensively studied (21,33–35). Cell tracking experiments reveal that mesenchymal prostate cancer cells exhibit increased general non-directed movement compared to epithelial cells derived from the same parent prostate cancer cell line in vitro (33). This increased movement phenotype is a direct product of the cell’s intrinsic properties, predisposing it to a certain behavior.…”

Section: Movement Ability Is Essential For Mobile Foraging Of Pre-metmentioning

confidence: 99%

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Revisiting Seed and Soil: Examining the Primary Tumor and Cancer Cell Foraging in Metastasis

Groot

Roy

Brown

et al. 2017

Molecular Cancer Research

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Metastasis is the consequence of a cancer cell that disperses from the primary tumor, travels throughout the body, and invades and colonizes a distant site. Based on Paget’s 1889 hypothesis, the majority of modern metastasis research focuses on the properties of the metastatic “seed and soil,” but the implications of the primary tumor “soil” have been largely neglected. The rare lethal metastatic “seed” arises as a result of the selective pressures in the primary tumor. Optimal foraging theory describes how cancer cells adopt a mobile foraging strategy to balance predation risk and resource reward. Further selection in the dispersal corridors leading out of the primary tumor enhances the adaptive profile of the potentially metastatic cell. This review focuses on the selective pressures of the primary tumor “soil” that generate lethal metastatic “seeds” which is essential to understanding this critical component of prostate cancer metastasis. Implications Elucidating the selective pressures of the primary tumor “soil” that generate lethal metastatic “seeds” is essential to understand how and why metastasis occurs in prostate cancer.

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Section: Optimal Foraging Of Prostate Cancermentioning

confidence: 99%

Section: Movement Ability Is Essential For Mobile Foraging Of Pre-metmentioning

confidence: 99%

Revisiting Seed and Soil: Examining the Primary Tumor and Cancer Cell Foraging in Metastasis

Groot

Roy

Brown

et al. 2017

Molecular Cancer Research

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“…Aerobic glycolysis contributes to the diverse aspects of tumor development, progression and prognosis [89, 137, 138]. The reversing the Warburg effect greatly compromises the tumorigenicity of tumor cells [139, 140], suggesting that targeting the metabolic changes could be an effective strategy for cancer treatment.…”

Section: Potential Targets For Tumor Therapymentioning

confidence: 99%

The sweet trap in tumors: aerobic glycolysis and potential targets for therapy

Chen

Wang

et al. 2016

Oncotarget

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Metabolic change is one of the hallmarks of tumor, which has recently attracted a great of attention. One of main metabolic characteristics of tumor cells is the high level of glycolysis even in the presence of oxygen, known as aerobic glycolysis or the Warburg effect. The energy production is much less in glycolysis pathway than that in tricarboxylic acid cycle. The molecular mechanism of a high glycolytic flux in tumor cells remains unclear. A large amount of intermediates derived from glycolytic pathway could meet the biosynthetic requirements of the proliferating cells. Hypoxia-induced HIF-1α, PI3K-Akt-mTOR signaling pathway, and many other factors, such as oncogene activation and tumor suppressor inactivation, drive cancer cells to favor glycolysis over mitochondrial oxidation. Several small molecules targeting glycolytic pathway exhibit promising anticancer activity both in vitro and in vivo. In this review, we will focus on the latest progress in the regulation of aerobic glycolysis and discuss the potential targets for the tumor therapy.

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“…In a normal prostate epithelial cell, E-cadherin is also connected internally with actin filaments 26. Changes in the cytoskeleton are most evident within the intermediate filaments, which changes from keratin to vimentin (VIM) providing the mesenchymal cells with their structure and contributing to motility 2728…”

Section: Emt In Pcamentioning

confidence: 99%

Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins

et al. 2016

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A striking characteristic of cancer cells is their remarkable phenotypic plasticity, which is the ability to switch states or phenotypes in response to environmental fluctuations. Phenotypic changes such as a partial or complete epithelial to mesenchymal transition (EMT) that play important roles in their survival and proliferation, and development of resistance to therapeutic treatments, are widely believed to arise due to somatic mutations in the genome. However, there is a growing concern that such a deterministic view is not entirely consistent with multiple lines of evidence, which indicate that stochasticity may also play an important role in driving phenotypic plasticity. Here, we discuss how stochasticity in protein interaction networks (PINs) may play a key role in determining phenotypic plasticity in prostate cancer (PCa). Specifically, we point out that the key players driving transitions among different phenotypes (epithelial, mesenchymal, and hybrid epithelial/mesenchymal), including ZEB1, SNAI1, OVOL1, and OVOL2, are intrinsically disordered proteins (IDPs) and discuss how plasticity at the molecular level may contribute to stochasticity in phenotypic switching by rewiring PINs. We conclude by suggesting that targeting IDPs implicated in EMT in PCa may be a new strategy to gain additional insights and develop novel treatments for this disease, which is the most common form of cancer in adult men.

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Glycolysis is the primary bioenergetic pathway for cell motility and cytoskeletal remodeling in human prostate and breast cancer cells

Cited by 156 publications

References 44 publications

Revisiting Seed and Soil: Examining the Primary Tumor and Cancer Cell Foraging in Metastasis

Revisiting Seed and Soil: Examining the Primary Tumor and Cancer Cell Foraging in Metastasis

The sweet trap in tumors: aerobic glycolysis and potential targets for therapy

Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins

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