The potential role of leptin in tumor invasion and metastasis

Red: Tumor-promoting effect. Blue: Dual role (tumor–suppressor or −promoting effect depending on the situation). CAFs: Cancer-associated fibroblasts, CTGF: Connective tissue growth factor, EGFR: Epidermal growth factor receptor, EMT: Epithelial–mesenchymal transition, ERK1/2: Extracellular signal-re...

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Bibliographic Details
Published in:Cytokine & growth factor reviews Vol. 38; pp. 80 - 97
Main Authors: Ray, Amitabha, Cleary, Margot P.
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01.12.2017
Subjects:
Invasive cancer
Leptin
Metastasis
Obesity
Prognosis
TAM
MCP-1
Prognosis
Metastasis
TNF
EGFR
CTGF
TNM
PI3K
Invasive cancer
Ob-R
Obesity
IL
HIF
ICAM
NSCLC
VEGF
CAF
IGF
AKT
EMT
ER
ECM
MMP
STAT
TGF
JAK
Leptin
ERK
ISSN:1359-6101, 1879-0305, 1879-0305
Online Access:Get full text
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Abstract Red: Tumor-promoting effect. Blue: Dual role (tumor–suppressor or −promoting effect depending on the situation). CAFs: Cancer-associated fibroblasts, CTGF: Connective tissue growth factor, EGFR: Epidermal growth factor receptor, EMT: Epithelial–mesenchymal transition, ERK1/2: Extracellular signal-regulated kinases 1 and 2, HER2: Human epidermal growth factor receptor 2, HIF-1α: Hypoxia-inducible factor-1 alpha, IGF-I: Insulin-like growth factor-I, JAK2: Janus kinase 2, MMPs: Matrix metalloproteinases, NF-κB: Nuclear factor-kappa B, Ob-R: Leptin receptor, PI3K: Phosphatidylinositol 3-kinase, STAT3: Signal transducer and activator of transcription 3, TAMs: Tumor-associated macrophages, TGF-β: Transforming growth factor-beta, VEGF: Vascular endothelial growth factor. [Display omitted] •In the tumor microenvironment leptin impacts intracellular signaling which may accelerate cancer cell migration and metastasis.•Leptin plays a role in cancers of the digestive and reproductive systems, which are a major burden of neoplastic disease worldwide.•Elevated serum leptin affects the prognosis of both adenocarcinomas and squamous cell carcinomas.•Several cancer dissemination mechanisms have been documented to be linked with leptin. The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin’s association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin's potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.
AbstractList The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin's association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin's potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin's association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin's potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.
The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin’s association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin’s potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients. Leptin-linked Pathological Mechanisms in Tumor Proliferation and Migration Red: Tumor-promoting effect Blue: Dual role (tumor–suppressor or –promoting effect depending on the situation) CAFs: Cancer-associated fibroblasts, CTGF: Connective tissue growth factor, EGFR: Epidermal growth factor receptor, EMT: Epithelial–mesenchymal transition, ERK1/2: Extracellular signal-regulated kinases 1 and 2, HER2: Human epidermal growth factor receptor 2, HIF-1α: Hypoxia-inducible factor-1 alpha, IGF-I: Insulin-like growth factor-I, JAK2: Janus kinase 2, MMPs: Matrix metalloproteinases, NF-κB: Nuclear factor-kappa B, Ob-R: Leptin receptor, PI3K: Phosphatidylinositol 3-kinase, STAT3: Signal transducer and activator of transcription 3, TAMs: Tumor-associated macrophages, TGF-β: Transforming growth factor-beta, VEGF: Vascular endothelial growth factor
Red: Tumor-promoting effect. Blue: Dual role (tumor–suppressor or −promoting effect depending on the situation). CAFs: Cancer-associated fibroblasts, CTGF: Connective tissue growth factor, EGFR: Epidermal growth factor receptor, EMT: Epithelial–mesenchymal transition, ERK1/2: Extracellular signal-regulated kinases 1 and 2, HER2: Human epidermal growth factor receptor 2, HIF-1α: Hypoxia-inducible factor-1 alpha, IGF-I: Insulin-like growth factor-I, JAK2: Janus kinase 2, MMPs: Matrix metalloproteinases, NF-κB: Nuclear factor-kappa B, Ob-R: Leptin receptor, PI3K: Phosphatidylinositol 3-kinase, STAT3: Signal transducer and activator of transcription 3, TAMs: Tumor-associated macrophages, TGF-β: Transforming growth factor-beta, VEGF: Vascular endothelial growth factor. [Display omitted] •In the tumor microenvironment leptin impacts intracellular signaling which may accelerate cancer cell migration and metastasis.•Leptin plays a role in cancers of the digestive and reproductive systems, which are a major burden of neoplastic disease worldwide.•Elevated serum leptin affects the prognosis of both adenocarcinomas and squamous cell carcinomas.•Several cancer dissemination mechanisms have been documented to be linked with leptin. The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin’s association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin's potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.
The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin's association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin's potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.
Author Cleary, Margot P.
Ray, Amitabha
AuthorAffiliation b The Hormel Institute, University of Minnesota, Austin, MN 55912
a Lake Erie College of Osteopathic Medicine, Seton Hill University, Greensburg, PA 15601
AuthorAffiliation_xml – name: a Lake Erie College of Osteopathic Medicine, Seton Hill University, Greensburg, PA 15601
– name: b The Hormel Institute, University of Minnesota, Austin, MN 55912
Author_xml – sequence: 1
  givenname: Amitabha
  surname: Ray
  fullname: Ray, Amitabha
  organization: Lake Erie College of Osteopathic Medicine, Seton Hill University, Greensburg, PA 15601, United States
– sequence: 2
  givenname: Margot P.
  surname: Cleary
  fullname: Cleary, Margot P.
  email: mpcleary@hi.umn.edu
  organization: The Hormel Institute, University of Minnesota, Austin, MN 55912, United States
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29158066$$D View this record in MEDLINE/PubMed
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Keywords TAM
MCP-1
Prognosis
Metastasis
TNF
EGFR
CTGF
TNM
PI3K
Invasive cancer
Ob-R
Obesity
IL
HIF
ICAM
NSCLC
VEGF
CAF
IGF
AKT
EMT
ER
ECM
MMP
STAT
TGF
JAK
Leptin
ERK
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Snippet Red: Tumor-promoting effect. Blue: Dual role (tumor–suppressor or −promoting effect depending on the situation). CAFs: Cancer-associated fibroblasts, CTGF:...
The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese...
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SubjectTerms Invasive cancer
Leptin
Metastasis
Obesity
Prognosis
Title The potential role of leptin in tumor invasion and metastasis
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https://dx.doi.org/10.1016/j.cytogfr.2017.11.002
https://www.ncbi.nlm.nih.gov/pubmed/29158066
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