THE EMERGING HALLMARKS OF CANCER METABOLISM

By N. Pavlova, Craig B. Thompson. Cell Metabolism, 2016

5,052 citations recorded by the source corpus.

Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and indirect consequence of oncogenic mutations. A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass. The alterations in intracellular and extracellular metabolites that can accompany cancer-associated metabolic reprogramming have profound effects on gene expression, cellular differentiation and the tumor microenvironment. In this Review, we have organized known cancer-associated metabolic changes into six hallmarks: (1) deregulated uptake of glucose and amino acids, (2) use of opportunistic modes of nutrient acquisition, (3) use of glycolysis/TCA cycle intermediates for biosynthesis and NADPH production, (4) increased demand for nitrogen, (5) alterations in metabolite-driven gene regulation, and (6) metabolic interactions with the microenvironment. While few tumors display all six hallmarks, most display several. The specific hallmarks exhibited by an individual tumor may ultimately contribute to better tumor classification and aid in directing treatment.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1e8b6414a84ad7a310eeee976435e51a609d3979

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Citations in the corpus

The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression (2019, background): “Furthermore, it can lead to radioresistance, impedes antitumor immunity, diminishes the effectiveness of basic chemotherapeutic drugs and may contribute to drug resistance via mTOR-signaling (Pavlova and Thompson 2016; Corbet and Feron 2017).”
Autophagy and Tumor Metabolism (2017, background): “…A uthor M anuscript A uthor M anuscript A uthor M anuscript Metabolism and Cancer It has long been known that cancers have altered metabolism to help meet the needs of cells that have the potential for unconstrained proliferation (Pavlova and Thompson, 2016; Vander Heiden and DeBerardinis, 2017).”
Fundamentals of cancer metabolism (2016, background): “Because some altered metabolic features are observed quite generally across many types of cancer cells, reprogrammed metabolism is considered a hallmark of cancer (1, 2).”
The role of m6A RNA methylation in cancer metabolism (2022, background): “In order to survive and adapt to these severe environmental pressures, cancer cells change their metabolic pathways to capture external metabolites and maximize the efficiency of metabolic enzymes [12].”
Oncogenic activation of PI3K-AKT-mTOR signaling suppresses ferroptosis via SREBP-mediated lipogenesis (2020, background): “Cancer cells usually endure elevated oxidative stress due to increased metabolic and proliferative burden (42, 43).”
Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “In order to systematically understand the role of metabolic reprogramming in cancer cells on establishing and maintaining a tumorigenic status, Pavlova & Thompson (2) summarized”
Glutamine Metabolism in Cancer: Understanding the Heterogeneity (2017, neutral): “Glutamine serves as an important source of reduced nitrogen for biosynthetic reactions, and as a source of carbon to replenish the tricarboxylic acid (TCA) cycle, produce glutathione, and serve as a precursor to nucleotide and lipid synthesis via reductive carboxylation (Figure 1) [1,2,6,7].”
Obesity shapes metabolism in the tumor microenvironment to suppress anti-tumor immunity (2020, background): “A hallmark feature of tumor cell metabolism is increased nutrient consumption tomeet energetic, anabolic, and pro-survival demands (Pavlova and Thompson, 2016; Spinelli and Haigis, 2018).”
Mitochondrial metabolism and cancer (2017, background): “, ATP citrate lyase (ACLY), is required for cancer cells to proliferate at optimal rates [85], but not for normal cells to do so (owing to a glucose-to-acetate metabolic switch) [86].”