The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

Gómez-Valenzuela, Fernán; Escobar, Elizabeth; Pérez‐Tomás, Ricardo; Montecinos, Viviana P.

doi:10.3389/fonc.2021.686792

Cited by 39 publications

(36 citation statements)

References 159 publications

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“…In the context of TME, regulatory T cells (Tregs) promote tumor development by dampening anti-tumor immune responses, whereas effector T cells promote inflammation. 71 ENO1 plays a key role in the regulation of T cell effector functions, including T cell activation 72 and the suppressive functions of induced Tregs. 73 Interestingly, downregulation of ENO1 activity represses the glycolytic activity of tumor-infiltrating CD8+ lymphocytes (CD8+ TILs), leading to their functional exhaustion.…”

Section: Eno1 Deregulates Cellular Energetics In Tumor Cellsmentioning

confidence: 99%

ENO1 and Cancer

Huang

Sun

Ping

2022

Molecular Therapy - Oncolytics

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a-Enolase (ENO1), also known as 2-phospho-D-glycerate hydrolase, is a glycolytic enzyme that catalyzes the conversion of 2-phosphoglyceric acid to phosphoenolpyruvic acid during glycolysis. It is a multifunctional oncoprotein that is present both in cell surface and cytoplasm, contributing to hit seven out of ten "hallmarks of cancer." ENO1's glycolytic function deregulates cellular energetic, sustains tumor proliferation, and inhibits cancer cell apoptosis. Moreover, ENO1 evades growth suppressors and helps tumors to avoid immune destruction. Besides, ENO1 "moonlights" on the cell surface and acts as a plasminogen receptor, promoting cancer invasion and metastasis by inducing angiogenesis. Overexpression of ENO1 on a myriad of cancer types together with its localization on the tumor surface makes it a great prognostic and diagnostic cancer biomarker as well as an accessible oncotherapeutic target. This review summarizes the up-todate knowledge about the relationship between ENO1 and cancer, examines ENO1's potential as a cancer biomarker, and discusses ENO1's role in novel onco-immunotherapeutic strategies. OVERVIEW OF ENO1 AND ITS ROLE IN CANCERENO1 is a multifunctional protein that partakes in various key intracellular and extracellular activities, depending on its localization (Figure 1). The primary function of ENO1 is to catalyze glycolysis; in

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Section: Eno1 Deregulates Cellular Energetics In Tumor Cellsmentioning

confidence: 99%

ENO1 and Cancer

Huang

Sun

Ping

2022

Molecular Therapy - Oncolytics

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“…In breast cancer there is a well-established paradigm of elevated COX-2, low 15-PGDH, increased PGE 2 , and associations with more aggressive disease and negative outcomes ( 43 , 44 , 46 – 49 ). COX-2 overexpression induces tumorigenesis via PGE 2 production, increased angiogenesis ( 42 ), and suppressed tumor immunity ( 40 , 43 – 45 , 50 , 51 ). In patient tumors, COX-2 overexpression is associated with poor prognoses and lower distant disease-free survival time ( 52 ).…”

Section: Prostaglandin E2 In Cancermentioning

confidence: 99%

“…As the primary mediator of the oncogenic effects of COX-2, PGE 2 -induced receptor signaling contributes to almost all of the major cancer hallmarks, including angiogenesis, proliferation, epithelial-mesenchymal transition (EMT), and the maintenance of CSC characteristics (42,43). PGE 2 is the most common prostanoid in the tumor microenvironment (44,45). In breast cancer there is a well-established paradigm of elevated COX-2, low 15-PGDH, increased PGE 2 , and associations with more aggressive disease and negative outcomes (43,44,(46)(47)(48)(49).…”

Section: Prostaglandin E2 In Cancermentioning

confidence: 99%

The Prostaglandin E2 Pathway and Breast Cancer Stem Cells: Evidence of Increased Signaling and Potential Targeting

et al. 2022

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Culprits of cancer development, metastasis, and drug resistance, cancer stem cells (CSCs) are characterized by specific markers, active developmental signaling pathways, metabolic plasticity, increased motility, invasiveness, and epithelial-mesenchymal transition. In breast cancer, these cells are often more prominent in aggressive disease, are amplified in drug-resistant tumors, and contribute to recurrence. For breast cancer, two distinct CSC populations exist and are typically defined by CD44+/CD24- cell surface marker expression or increased aldehyde dehydrogenase (ALDH) activity. These CSC populations share many of the same properties but also exhibit signaling pathways that are more active in CD44+/CD24- or ALDH+ populations. Understanding these CSC populations and their shared or specific signaling pathways may lead to the development of novel therapeutic strategies that will improve breast cancer patient outcomes. Herein, we review the current evidence and assess published patient tumor datasets of sorted breast CSC populations for evidence of heightened prostaglandin E2 (PGE2) signaling and activity in these breast CSC populations. PGE2 is a biologically active lipid mediator and in cancer PGE2 promotes tumor progression and poor patient prognosis. Overall, the data suggests that PGE2 signaling is important in propagating breast CSCs by enhancing inherent tumor-initiating capacities. Development of anti-PGE2 signaling therapeutics may be beneficial in inhibiting tumor growth and limiting breast CSC populations.

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“…Nevertheless, it has also been described that in a previously detected tumor, not linked to a previous inflammatory process, inflammation is present in the surrounding area of the tumor, promoting cancer progression to achieve the malignant phenotype, tissue remodeling, metastasis, and angiogenesis, or the suppression of immune response [97]. Regarding microenvironmental components, it has been reported that macrophages are the most abundant cells in tumor environments and their function in cancer is contradictory.…”

Section: Inflammation and Cancermentioning

confidence: 99%

Anti-Inflammatory and Anticancer Effects of Microalgal Carotenoids

et al. 2021

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Acute inflammation is a key component of the immune system’s response to pathogens, toxic agents, or tissue injury, involving the stimulation of defense mechanisms aimed to removing pathogenic factors and restoring tissue homeostasis. However, uncontrolled acute inflammatory response may lead to chronic inflammation, which is involved in the development of many diseases, including cancer. Nowadays, the need to find new potential therapeutic compounds has raised the worldwide scientific interest to study the marine environment. Specifically, microalgae are considered rich sources of bioactive molecules, such as carotenoids, which are natural isoprenoid pigments with important beneficial effects for health due to their biological activities. Carotenoids are essential nutrients for mammals, but they are unable to synthesize them; instead, a dietary intake of these compounds is required. Carotenoids are classified as carotenes (hydrocarbon carotenoids), such as α- and β-carotene, and xanthophylls (oxygenate derivatives) including zeaxanthin, astaxanthin, fucoxanthin, lutein, α- and β-cryptoxanthin, and canthaxanthin. This review summarizes the present up-to-date knowledge of the anti-inflammatory and anticancer activities of microalgal carotenoids both in vitro and in vivo, as well as the latest status of human studies for their potential use in prevention and treatment of inflammatory diseases and cancer.

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The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition

Cited by 39 publications

References 159 publications

ENO1 and Cancer

ENO1 and Cancer

The Prostaglandin E2 Pathway and Breast Cancer Stem Cells: Evidence of Increased Signaling and Potential Targeting

Anti-Inflammatory and Anticancer Effects of Microalgal Carotenoids

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