Leptin induces CREB-dependent aromatase activation through COX-2 expression in breast cancer cells

Kim, Hyung Gyun; Jin, Sun Woo; Kim, Yong An; Khanal, Tilak; Lee, Gi Ho; Kim, Se Jong; Rhee, Sang Dal; Chung, Young Chul; Hwang, Young Jung; Jeong, Tae Cheon; Jeong, Hye Gwang

doi:10.1016/j.fct.2017.05.058

Cited by 24 publications

(22 citation statements)

References 44 publications

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“…Although the underlying mechanisms are still unclear, both leptin and its receptor expression and function have been positively correlated with cancer progression in some endocrine-related cancers [ 137 ] and this effect seems to be mainly mediated by LEPR activation of PI3K, ERK1/2 and Jak2/Stat3 signaling pathways [ 138 , 139 , 140 , 141 ]. These pathways regulate the expression of several cancers related genes such as cyclin D1, COX-2, VEGF and potentiates several procarcinogenic processes including angiogenesis, antiapoptosis, cell proliferation, migration and mesenchymal transformation [ 142 , 143 , 144 ]. This contributes to various steps of tumor progression, from cancer stem cell activity, survival, growth and proliferation to metastatic invasion in different types of cancer cells [ 145 , 146 , 147 , 148 , 149 , 150 ].…”

Section: Leptin As a Mediator Of Inflammationmentioning

confidence: 99%

Role of Leptin in Inflammation and Vice Versa

Pérez-Pérez

Sánchez-Jiménez

Vilariño-García

et al. 2020

IJMS

169

116

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Inflammation is an essential immune response for the maintenance of tissue homeostasis. In a general sense, acute and chronic inflammation are different types of adaptive response that are called into action when other homeostatic mechanisms are insufficient. Although considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and tissue injury, the causes and mechanisms of systemic chronic inflammation are much less known. The pathogenic capacity of this type of inflammation is puzzling and represents a common link of the multifactorial diseases, such as cardiovascular diseases and type 2 diabetes. In recent years, interest has been raised by the discovery of novel mediators of inflammation, such as microRNAs and adipokines, with different effects on target tissues. In the present review, we discuss the data emerged from research of leptin in obesity as an inflammatory mediator sustaining multifactorial diseases and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses. On the other direction, chronic inflammation, either from autoimmune or infectious diseases, or impaired microbiota (dysbiosis) may impair the leptin response inducing resistance to the weight control, and therefore it may be a cause of obesity. Thus, we are reviewing the published data regarding the role of leptin in inflammation, and the other way around, the role of inflammation on the development of leptin resistance and obesity

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Section: Leptin As a Mediator Of Inflammationmentioning

confidence: 99%

Role of Leptin in Inflammation and Vice Versa

Pérez-Pérez

Sánchez-Jiménez

Vilariño-García

et al. 2020

IJMS

169

116

View full text Add to dashboard Cite

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“…BDNF plays a key role in the CNS through binding its receptor. Administration of leptin to the hindbrain significantly increases the level of BDNF within the dorsal vagal complex (Sahu et al, 2016; Kim et al, 2017).…”

Section: Leptin’s Neurotrophic Effectmentioning

confidence: 99%

“…ERK1/2 phosphorylation (pERK1/2) can directly activate the protein signaling cascade to regulate a series of cellular processes, such as nerve growth, survival and neuroplasticity. Leptin can induce ERK1/2 phosphorylation in a time-dependent manner (Kim et al, 2017; Ghasemi et al, 2018; Han et al, 2018). The increase in pERK1/2 can phosphorylate CREB and alter its transcriptional activity, which is considered a key event of cell survival and cognition (Liu et al, 2015) and in the case of cocultured neurons and astrocytes, leptin exerts an anti-apoptotic effect in astrocytes against glutamate toxicity (Park et al, 2017).…”

Section: Leptin’s Neurotrophic Effectmentioning

confidence: 99%

Role of Leptin in Mood Disorder and Neurodegenerative Disease

et al. 2019

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The critical regulatory role of leptin in the neuroendocrine system has been widely reported. Significantly, leptin can improve learning and memory, affect hippocampal synaptic plasticity, exert neuroprotective efficacy and reduce the risk of several neuropsychiatric diseases. In terms of depression, leptin could modulate the levels of neurotransmitters, neurotrophic factors and reverse the dysfunction in the hypothalamic-pituitary-adrenal axis (HPA). At the same time, leptin affects neurological diseases during the regulation of metabolic homeostasis. With regards to neurodegenerative diseases, leptin can affect them via neuroprotection, mainly including Alzheimer’s disease and Parkinson’s disease. This review will summarize the mechanisms of leptin signaling within the neuroendocrine system with respect to these diseases and discuss the therapeutic potential of leptin.

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“…Obesity leads to higher levels of leptin which promotes BC progression through JAK/STAT3 and estrogen pathways . The adipose derived stromal cells (ADSCs) harbor leptin receptors and mediate estrogenic effects in response to paracrine and/or autocrine stimulation by leptin . The aromatase, which is involved in E2 synthesis, is mainly expressed in adipose tissue .…”

Section: Determinants Of Bc Risk: Considerations For Bc Prevention Anmentioning

confidence: 99%

“…67 The adipose derived stromal cells (ADSCs) harbor leptin receptors and mediate estrogenic effects in response to paracrine and/or autocrine stimulation by leptin. [68][69][70] The aromatase, which is involved in E2 synthesis, is mainly expressed in adipose tissue. 71 The estrogen precursor d-4-androstenedione is converted into E2 by the enzymatic action of aromatase in ADSCs.…”

Section: Determinants Of Bc Risk: Considerations For Bc Prevention Anmentioning

confidence: 99%

Translational opportunities for broad‐spectrum natural phytochemicals and targeted agent combinations in breast cancer

Nagaprashantha

Adhikari

Singhal

et al. 2017

Intl Journal of Cancer

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Breast cancer (BC) prevention and therapy in the context of life-style risk factors and biological drivers is a major focus of developmental therapeutics in oncology. Obesity, alcohol, chronic estrogen signaling and smoking have distinct BC precipitating and facilitating effects that may act alone or in combination. A spectrum of signaling events including enhanced oxidative stress and changes in estrogen-receptor (ER)-dependent and -independent signaling drive the progression of BC. Breast tumors modulate ERα/ERβ ratio, upregulate proliferative pathways driven by ERα and HER2 with a parallel loss and/or downregulation of tumor suppressors such as TP53 and PTEN which together impact the efficacy of therapeutic strategies and frequently lead to emergence of drug resistance. Natural phytochemicals modulate oxidative stress, leptin, integrin, HER2, MAPK, ERK, Wnt/β-catenin and NFκB signaling along with regulating ERα and ERβ, thereby presenting unique opportunities for both primary and combinatorial interventions in BC. In this regard, this article focuses on critical analyses of the evidence from multiple studies on the efficacy of natural phytochemicals in BC. In addition, areas in which the combinations of such effective natural phytochemicals with approved and/or developing anticancer agents can be translationally beneficial are discussed to derive evidence-based inference for addressing challenges in BC control and therapy.

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Leptin induces CREB-dependent aromatase activation through COX-2 expression in breast cancer cells

Cited by 24 publications

References 44 publications

Role of Leptin in Inflammation and Vice Versa

Role of Leptin in Inflammation and Vice Versa

Role of Leptin in Mood Disorder and Neurodegenerative Disease

Translational opportunities for broad‐spectrum natural phytochemicals and targeted agent combinations in breast cancer

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