A proteomic glimpse into the oncogenesis of prostate cancer

Martiny, Patrícia Borba; Alcoba, Diego Duarte; Neto, Brasil Silva; Carvalho, Paulo C.; Brum, Ilma Simoni

doi:10.1016/j.jab.2018.05.003

Cited by 4 publications

(2 citation statements)

References 56 publications

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“…Nevertheless, two features of the Warburg effect remain unaltered: increased glucose uptake and lactate production [6,7]. Aerobic glycolysis is markedly heightened in over 70% of cancer types, such as lung [8], breast [9], liver [10,11], brain [12], prostate [13], gynecologic [14], and pancreatic cancer [4,15,16]. Similar to solid tumors, hematologic malignancies, such as lymphomas [16][17][18] and leukemias [16,19,20], also demonstrate high aerobic glycolysis and low OXPHOS rates.…”

Section: Introductionmentioning

confidence: 99%

Targeting the Metabolic Paradigms in Cancer and Diabetes

Bosso,

Haddad,

Al Madhoun

et al. 2024

Biomedicines

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Dysregulated metabolic dynamics are evident in both cancer and diabetes, with metabolic alterations representing a facet of the myriad changes observed in these conditions. This review delves into the commonalities in metabolism between cancer and type 2 diabetes (T2D), focusing specifically on the contrasting roles of oxidative phosphorylation (OXPHOS) and glycolysis as primary energy-generating pathways within cells. Building on earlier research, we explore how a shift towards one pathway over the other serves as a foundational aspect in the development of cancer and T2D. Unlike previous reviews, we posit that this shift may occur in seemingly opposing yet complementary directions, akin to the Yin and Yang concept. These metabolic fluctuations reveal an intricate network of underlying defective signaling pathways, orchestrating the pathogenesis and progression of each disease. The Warburg phenomenon, characterized by the prevalence of aerobic glycolysis over minimal to no OXPHOS, emerges as the predominant metabolic phenotype in cancer. Conversely, in T2D, the prevailing metabolic paradigm has traditionally been perceived in terms of discrete irregularities rather than an OXPHOS-to-glycolysis shift. Throughout T2D pathogenesis, OXPHOS remains consistently heightened due to chronic hyperglycemia or hyperinsulinemia. In advanced insulin resistance and T2D, the metabolic landscape becomes more complex, featuring differential tissue-specific alterations that affect OXPHOS. Recent findings suggest that addressing the metabolic imbalance in both cancer and diabetes could offer an effective treatment strategy. Numerous pharmaceutical and nutritional modalities exhibiting therapeutic effects in both conditions ultimately modulate the OXPHOS–glycolysis axis. Noteworthy nutritional adjuncts, such as alpha-lipoic acid, flavonoids, and glutamine, demonstrate the ability to reprogram metabolism, exerting anti-tumor and anti-diabetic effects. Similarly, pharmacological agents like metformin exhibit therapeutic efficacy in both T2D and cancer. This review discusses the molecular mechanisms underlying these metabolic shifts and explores promising therapeutic strategies aimed at reversing the metabolic imbalance in both disease scenarios.

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Section: Introductionmentioning

confidence: 99%

Targeting the Metabolic Paradigms in Cancer and Diabetes

Bosso,

Haddad,

Al Madhoun

et al. 2024

Biomedicines

View full text Add to dashboard Cite

show abstract

“…Nevertheless, the two following features remain unaltered with regard to the Warburg effect: increased glucose uptake and lactate production [5,6]. Aerobic glycolysis is markedly heightened in over 70% of cancer types such as lung [7], breast [8], liver [9,10], brain [11], prostate [12], gynecologic [13], and pancreatic cancer [3,14,15]. Similar to solid tumors, hematologic malignancies, such as lymphomas [15][16][17] and leukemias [15,18,19], also demonstrate high aerobic glycolysis and low OXPHOS rates.…”

Section: Introductionmentioning

confidence: 99%

Targeting the Metabolic Paradigms in Cancer and Diabetes

Bosso,

Haddad,

Al Madhoun

et al. 2023

Preprint

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As yin and yang, cancer and diabetes are metabolic disorders characterized by deregulated, yet opposing, metabolic alterations. These metabolic shifts reflect a complex network of defective underlying signaling pathways, which ultimately orchestrate both disease pathogenesis and progression. The Warburg effect portrays the chief metabolic phenotype in cancer and is reflected by the dominance of aerobic glycolysis over minimal-to-no viable oxidative phosphorylation in cancer. Conversely, during the pathogenesis of type 2 diabetes (T2D), oxidative phosphorylation is constantly heightened. In advanced insulin resistance and T2D, the metabolic landscape becomes more complex, with exacerbating metabolic alterations affecting oxidative phosphorylation in a tissue-specific manner. Promising nutritional adjuvants, such as alpha-lipoic acid and flavonoids, can reprogram metabolism and exert antitumor and antidiabetic effects. Other pharmacological agents, such as metformin, have therapeutic effects on cancer and T2D. Herein, we discuss the molecular mechanisms and signaling pathways involved in the metabolic shifts in cancer and T2D, and explore the therapeutic strategies under investigation that aim to reverse the metabolic shift in both disease scenarios.

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Water as a reactant in the differential expression of proteins in cancer

Dick¹

2020

Preprint

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The large amounts of proteomic data now available for cancer can used to investigate whether the physicochemical conditions of tumors are reflected in patterns of protein expression and chemical composition. Compositional analysis of more than 250 datasets for differentially expressed proteins compiled from the literature reveals a clear signal of higher stoichiometric hydration state (n H 2 O , derived from the theoretical formation reactions of proteins from particular basis species) in specific cancer types compared to normal tissue; this trend is also evident in pan-cancer transcriptomic and proteomic datasets from The Cancer Genome Atlas and Human Protein Atlas. In marked contrast to cancer, n H 2 O decreases for differentially expressed proteins in hyperosmotic stress (including high glucose) experiments and 3D cell culture compared to monolayer growth. Compositional analysis combined with gene ages (phylostrata) taken from the literature shows higher n H 2 O of human proteins earlier in evolution. Further analyses using amino acid biosynthetic reactions supports the conclusion that a net increase of water going into the reactions of protein synthesis is a biochemical characteristic shared by most cancer types. These findings raise the possibility of a basic physicochemical link between increased water content in tumors and the atavistic or embryonic patterns of gene and protein expression in cancer.

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A proteomic glimpse into the oncogenesis of prostate cancer

Cited by 4 publications

References 56 publications

Targeting the Metabolic Paradigms in Cancer and Diabetes

Targeting the Metabolic Paradigms in Cancer and Diabetes

Targeting the Metabolic Paradigms in Cancer and Diabetes

Water as a reactant in the differential expression of proteins in cancer

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