The Intricate Interplay between Mechanisms Underlying Aging and Cancer

Piano, Amanda; Titorenko, Vladimir I.

doi:10.14336/ad.2014.0209

Cited by 23 publications

(21 citation statements)

References 298 publications

(309 reference statements)

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“…In our study, only 7% of all participants believed chemical or occupational exposure might have caused their disease, and a mere 8% of occupationally exposed participants mentioned this as a cause, even though certain types of occupational exposure are established risk factors. Surprisingly, none of our participants mentioned ageing even though this is an established risk factor for cancer in general [20,21]. An explanation may be that only patients younger than 75 were recruited.…”

Section: Stratificationmentioning

confidence: 75%

Low awareness of risk factors among bladder cancer survivors: New evidence and a literature overview

Westhoff¹,

Oliveira-Neumayer²,

Aben

et al. 2016

European Journal of Cancer

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Most UBC survivors did not suspect any cause that might have contributed to the development of their cancer. Even among participants with established risk factors for bladder cancer, these risk factors were not commonly perceived. This finding probably reflects the superficial knowledge of risk factors for bladder cancer in the population and highlights the importance of effective education on cancer prevention.

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Section: Stratificationmentioning

confidence: 75%

Low awareness of risk factors among bladder cancer survivors: New evidence and a literature overview

Westhoff¹,

Oliveira-Neumayer²,

Aben

et al. 2016

European Journal of Cancer

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“…Among such diseases are arthritis, diabetes, heart disease, kidney disease, liver dysfunction, sarcopenia, stroke, neurodegenerative diseases (including Parkinson's, Alzheimer's and Huntington's diseases), and many forms of cancer [3, 6, 9, 12, 15–18, 21, 79, 94–105]. Because the major aspects of aging and age-related pathology are conserved across phyla [1, 4–6, 10–13, 16–18], it is noteworthy that this study, recent findings [78] and our ongoing research have revealed several features of the six PEs as potential interventions for decelerating chronic diseases of old age.…”

Section: Discussionmentioning

confidence: 99%

Six plant extracts delay yeast chronological aging through different signaling pathways

et al. 2016

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Our recent study has revealed six plant extracts that slow yeast chronological aging more efficiently than any chemical compound yet described. The rate of aging in yeast is controlled by an evolutionarily conserved network of integrated signaling pathways and protein kinases. Here, we assessed how single-gene-deletion mutations eliminating each of these pathways and kinases affect the aging-delaying efficiencies of the six plant extracts. Our findings imply that these extracts slow aging in the following ways: 1) plant extract 4 decreases the efficiency with which the pro-aging TORC1 pathway inhibits the anti-aging SNF1 pathway; 2) plant extract 5 mitigates two different branches of the pro-aging PKA pathway; 3) plant extract 6 coordinates processes that are not assimilated into the network of presently known signaling pathways/protein kinases; 4) plant extract 8 diminishes the inhibitory action of PKA on SNF1; 5) plant extract 12 intensifies the anti-aging protein kinase Rim15; and 6) plant extract 21 inhibits a form of the pro-aging protein kinase Sch9 that is activated by the pro-aging PKH1/2 pathway.

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“…Other authors have shown that knockdown of RBP4 significantly reduces ovarian cancer cell migration and proliferation driven through the RhoA/Rock1 and extracellular signal-regulated kinase (ERK) pathways [26].The aim of our studies was to explain the role of RBP4 protein in the growth and metastatic spread of two murine breast cancer isogenic cell lines (derived from a single tumor of BALB/c mouse); metastatic 4T1 and nonmetastatic 67NR, representing basal-like and luminal-like phenotype, respectively [2,4]. Moreover, because, in many cases, cancer is associated with the aging process (largely reviewed in [27]) and aging affects the metastatic phenotype of cancer cells as well as tumor angiogenesis [28][29][30], we decided to include in our studies young and aged animals. To the best of our knowledge, no previous studies have investigated the effect of RBP4 protein on the metastatic spread of cancer.…”

mentioning

confidence: 99%

Retinol-Binding Protein 4 Accelerates Metastatic Spread and Increases Impairment of Blood Flow in Mouse Mammary Gland Tumors

Papiernik

Urbaniak

Kłopotowska

et al. 2020

Cancers

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Retinol-binding protein 4 (RBP4) is proposed as an adipokine that links obesity and cancer. We analyzed the role of RBP4 in metastasis of breast cancer in patients and in mice bearing metastatic 4T1 and nonmetastatic 67NR mammary gland cancer. We compared the metastatic and angiogenic potential of these cells transduced with Rbp4 (4T1/RBP4 and 67NR/RBP4 cell lines). Higher plasma levels of RBP4 were observed in breast cancer patients with metastatic tumors than in healthy donors and patients with nonmetastatic cancer. Increased levels of RBP4 were observed in plasma, tumor tissue, liver, and abdominal fat. Moreover, the blood vessel network was highly impaired in mice bearing 4T1 as compared to 67NR tumors. RBP4 transductants showed further impairment of blood flow and increased metastatic potential. Exogenous RBP4 increased lung settlement by 67NR and 4T1 cells. In vitro studies showed increased invasive and clonogenic potential of cancer cells treated with or overexpressing RBP4. This effect is not dependent on STAT3 phosphorylation. RBP4 enhances the metastatic potential of breast cancer tumors through a direct effect on cancer cells and through increased endothelial dysfunction and impairment of blood vessels within the tumor.Cancers 2020, 12, 623 2 of 21 cancer pulmonary metastasis. These processes precede the onset of a phenotypic switch in the lung endothelium toward a mesenchymal phenotype (EndMT), which is parallel to the appearance of the first pulmonary metastatic colonies [7]. Therefore, therapeutic strategies that aim to normalize endothelial dysfunction can decrease the metastatic potential of this type of breast cancer [8][9][10].Apart from its involvement in cancer development, endothelial dysfunction plays an important role in the development of cardiovascular diseases and atherosclerosis. Moreover, in type 2 diabetes mellitus, endothelial dysfunction and insulin resistance often coexist at the earliest stage of atherosclerosis with elevation of serum retinol-binding protein 4 (RBP4), a specific retinol transporter in the blood [11]. It is documented that RBP4 induces inflammation of endothelial cells in vitro. This action is due to the stimulation of proinflammatory molecules involved in leukocyte recruitment and their adherence to endothelium, and it is independent of retinol and the RBP4 membrane receptor STRA6 [12]. Endothelial inflammation induced by RBP4 is largely mediated by toll-like receptor 4 (TLR4), and in part, through the c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways [13]. Moreover, in isolated aorta rings, RBP4 treatment significantly increased NO production, stimulating the PI3K/Akt/eNOS pathway [14].RBP4, classified as adipokine [15], is proposed as the protein linking obesity and cancer [16]. Studies have shown various correlations between RBP4 plasma/tumor tissue levels and the development of certain types of cancer. For instance, Fei et al. reported lower RBP4 serum levels in patients with colon cancer than in healthy individu...

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The Intricate Interplay between Mechanisms Underlying Aging and Cancer

Cited by 23 publications

References 298 publications

Low awareness of risk factors among bladder cancer survivors: New evidence and a literature overview

Low awareness of risk factors among bladder cancer survivors: New evidence and a literature overview

Six plant extracts delay yeast chronological aging through different signaling pathways

Retinol-Binding Protein 4 Accelerates Metastatic Spread and Increases Impairment of Blood Flow in Mouse Mammary Gland Tumors

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