Cancer Metabolism and the Evasion of Apoptotic Cell Death

Cancers, Journal Year: 2019, Volume and Issue: 11(8), P. 1144 - 1144

Published: Aug. 9, 2019

Cellular growth and proliferation depend upon the acquisition synthesis of specific metabolites. These metabolites fuel bioenergy, biosynthesis, redox potential required for duplication cellular biomass. Multicellular organisms maintain tissue homeostasis by balancing signals promoting removal cells via apoptosis. While apoptosis is in itself an energy dependent process activated intrinsic extrinsic signals, whether nutrient (elevated or suppressed) their metabolism regulates less well investigated. Normal regulated lineage features microenvironment driven features. In context cancer, genetic abnormalities, unconventional microenvironments and/or therapy engage constitutive pro-survival signaling to re-program rewire survival, growth, proliferation. It thus becomes particularly relevant understand altered cancer can also contribute evasion consequently resistance. Our review attempts dissect a causal relationship between two hallmarks, i.e., deregulated energetics programmed cell death with primary focus on pathway

Language: Английский

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Tumor microenvironment signaling and therapeutics in cancer progression

Cancer Communications, Journal Year: 2023, Volume and Issue: 43(5), P. 525 - 561

Published: April 2, 2023

Abstract Tumor development and metastasis are facilitated by the complex interactions between cancer cells their microenvironment, which comprises stromal extracellular matrix (ECM) components, among other factors. Stromal can adopt new phenotypes to promote tumor cell invasion. A deep understanding of signaling pathways involved in cell‐to‐cell cell‐to‐ECM is needed design effective intervention strategies that might interrupt these interactions. In this review, we describe microenvironment (TME) components associated therapeutics. We discuss clinical advances prevalent newly discovered TME, immune checkpoints immunosuppressive chemokines, currently used inhibitors targeting pathways. These include both intrinsic non‐autonomous TME: protein kinase C (PKC) signaling, Notch, transforming growth factor (TGF‐β) Endoplasmic Reticulum (ER) stress response, lactate Metabolic reprogramming, cyclic GMP–AMP synthase (cGAS)–stimulator interferon genes (STING) Siglec also recent Programmed Cell Death Protein 1 (PD‐1), Cytotoxic T‐Lymphocyte Associated 4 (CTLA4), T‐cell immunoglobulin mucin‐3 (TIM‐3) Lymphocyte Activating Gene 3 (LAG3) checkpoint along with C‐C chemokine receptor (CCR4)‐ class chemokines 22 (CCL22)/ 17 (CCL17), type 2 (CCR2)‐ (C‐C motif) ligand (CCL2), 5 (CCR5)‐ (CCL3) axis TME. addition, review provides a holistic TME as three‐dimensional microfluidic models believed recapitulate original characteristics patient hence may be platform study mechanisms screen for various anti‐cancer therapies. further systemic influences gut microbiota reprogramming treatment response. Overall, comprehensive analysis diverse most critical highlighting newest preclinical studies underlying biology. highlight importance technologies microfluidics lab‐on‐chip research present an overview extrinsic factors, such inhabitant human microbiome, have potential modulate biology drug responses.

Language: Английский

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Reprogramming of glutamine metabolism and its impact on immune response in the tumor microenvironment

Cell Communication and Signaling, Journal Year: 2022, Volume and Issue: 20(1)

Published: July 27, 2022

Abstract Metabolic reprogramming and immune escape play a major role in tumorigenesis. Increasing number of studies have shown that glutamine metabolism is putative determinant the anti-tumor response tumor microenvironment (TME). Usually, predatory uptake by cells TME results limited utilization affects response. The cell-programmed partitioning also However, tumors modulates regulating PD-L1 expression. Likewise, their function. Additionally, different types inhibitors extensively regulate while suppressing cell proliferation. Herein, we discuss how metabolic regulates responses, as well functional changes context targeting metabolism, which can better explain potential combination with immunotherapy for cancer.

Language: Английский

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The Role of NRF2/KEAP1 Signaling Pathway in Cancer Metabolism

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(9), P. 4376 - 4376

Published: April 22, 2021

The nuclear factor-erythroid 2 p45-related factor (NRF2, also called

Language: Английский

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Microenvironmental ammonia enhances T cell exhaustion in colorectal cancer

Cell Metabolism, Journal Year: 2022, Volume and Issue: 35(1), P. 134 - 149.e6

Published: Dec. 16, 2022

Language: Английский

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