Regulation of vascular permeability in cancer metastasis

Tomita, Takeshi; Kato, Masayoshi; Hiratsuka, Sachie

doi:10.1111/cas.14942

Cited by 47 publications

(29 citation statements)

References 64 publications

(147 reference statements)

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“…The co-culture medium effectively recruited macrophages, demonstrating a potential mechanism of angiogenesis. Furthermore, vascular endothelial permeability was increased by fibrinogen in vitro, consistent with previous study [36][37][38]. We found that ICAM1 expression was induced by exogenous fibrinogen.…”

Section: Discussionsupporting

confidence: 92%

Fibrinogen promotes gallbladder cancer cell metastasis and extravasation by inducing ICAM1 expression

Jiang

et al. 2022

Med Oncol

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Fibrinogen (FIB) plays an important role in tumor progression. Here, we explored role of fibrinogen in gallbladder cancer (GBC) metastasis. The plasma fibrinogen level in M1 GBC patients was higher than in M0 GBC patients, indicating that fibrinogen may participate in GBC metastasis. Treatment of GBC cell lines with fibrinogen promoted metastasis and induced the expression of intercellular adhesion molecule 1 (ICAM1). ICAM1 overexpression promoted metastasis and knockdown inhibited it. The cell adhesion and transendothelial migration of GBC cells were enhanced by fibrinogen treatment and ICAM1 overexpression.In addition, the medium of fibrinogen-treated and overexpression-ICAM1 NOZ cells exhibited enhanced macrophages recruitment. This may work in concert to promote angiogenesis. Immunohistochemistry results on clinical specimens showed that higher fibrinogen levels, higher ICAM1 expression, higher blood vessel density, and higher macrophage levels were present simultaneously. Collectively, this study indicates fibrinogen promotes metastasis and extravasation by inducing ICAM1 expression to enhance tumor cell migration, cell adhesion, transendothelial migration and promote angiogenesis and increase vascular endothelial permeability.

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Section: Discussionsupporting

confidence: 92%

Fibrinogen promotes gallbladder cancer cell metastasis and extravasation by inducing ICAM1 expression

Jiang

et al. 2022

Med Oncol

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“…261 In addition, vascular inflammation caused by adipokines like leptin leads to elevated permeability, which is indispensable for cancer metastasis. 262 , 263 Finally, adipocytes can affect the biological behavior of carcinoma by modifying the extracellular matrix (ECM) structure which is characterized by a high degree of fibrosis in ATME. 264 Typically, the researchers observed an abundant fibrotic response in tumor areas that were enriched in adipocytes or located adjacent to adipose tissue.…”

Section: The Developmental Origin and Anatomical Location Of Thermoge...mentioning

confidence: 99%

The evolving view of thermogenic fat and its implications in cancer and metabolic diseases

Yin

Chen

Ruze

et al. 2022

Sig Transduct Target Ther

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The incidence of metabolism-related diseases like obesity and type 2 diabetes mellitus has reached pandemic levels worldwide and increased gradually. Most of them are listed on the table of high-risk factors for malignancy, and metabolic disorders systematically or locally contribute to cancer progression and poor prognosis of patients. Importantly, adipose tissue is fundamental to the occurrence and development of these metabolic disorders. White adipose tissue stores excessive energy, while thermogenic fat including brown and beige adipose tissue dissipates energy to generate heat. In addition to thermogenesis, beige and brown adipocytes also function as dynamic secretory cells and a metabolic sink of nutrients, like glucose, fatty acids, and amino acids. Accordingly, strategies that activate and expand thermogenic adipose tissue offer therapeutic promise to combat overweight, diabetes, and other metabolic disorders through increasing energy expenditure and enhancing glucose tolerance. With a better understanding of its origins and biological functions and the advances in imaging techniques detecting thermogenesis, the roles of thermogenic adipose tissue in tumors have been revealed gradually. On the one hand, enhanced browning of subcutaneous fatty tissue results in weight loss and cancer-associated cachexia. On the other hand, locally activated thermogenic adipocytes in the tumor microenvironment accelerate cancer progression by offering fuel sources and is likely to develop resistance to chemotherapy. Here, we enumerate current knowledge about the significant advances made in the origin and physiological functions of thermogenic fat. In addition, we discuss the multiple roles of thermogenic adipocytes in different tumors. Ultimately, we summarize imaging technologies for identifying thermogenic adipose tissue and pharmacologic agents via modulating thermogenesis in preclinical experiments and clinical trials.

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“…Tumor cells can bind to endothelial cells and induce EC necrosis via a TNF receptor family mechanism. Tumor cells can also release a large number of molecules that affect EC permeability [ 35 ].…”

Section: Vascular Permeability In Diseasesmentioning

confidence: 99%

Vascular Permeability in Diseases

Wautier

2022

IJMS

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Vascular permeability is a selective mechanism that maintains the exchange between vessels, tissues, and organs. The regulation was mostly studied during the nineteenth century by physiologists who defined physical laws and equations, taking blood, tissue interstitial, and oncotic pressure into account. During the last decades, a better knowledge of vascular cell functions and blood-vessel interactions opens a new area of vascular biology. Endothelial cell receptors vascular cell adhesion molecule (VCAM), intercellular cell adhesion molecule (ICAM), vascular endothelial growth factor receptor (VEGFR-2), receptor for advanced glycation end products (RAGE), and mediators were identified and their role in homeostasis and pathological situations was described. The molecular differences of endothelial cell junctions (tight, gap, and adherens junctions) and their role in vascular permeability were characterized in different organs. The main mediators of vasomotricity and permeability, such as prostaglandins, nitric oxide (NO), prostacyclin, vascular growth factor (VEGF), and cytokines, have been demonstrated to possess major functions in steady state and pathological situations. Leukocytes were shown to adhere to endothelium and migrate during inflammatory situations and infectious diseases. Increased vascular permeability is linked to endothelium integrity. Glycocalyx, when intact, may limit cancer cell metastasis. Biological modifications of blood and tissue constituents occurring in diabetes mellitus were responsible for increased permeability and, consequently, ocular and renal complications. Vascular pressure and fluidity are major determinants of pulmonary and cerebral edema. Beside the treatment of the infectious disease, of the blood circulation dysfunction and inflammatory condition, drugs (cyclooxygenase inhibitors) and specific antibodies anti-cytokine (anti-VEGF) have been demonstrated to reduce the severity and the mortality in diseases that exhibited enhanced vascular permeability.

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Regulation of vascular permeability in cancer metastasis

Cited by 47 publications

References 64 publications

Fibrinogen promotes gallbladder cancer cell metastasis and extravasation by inducing ICAM1 expression

Fibrinogen promotes gallbladder cancer cell metastasis and extravasation by inducing ICAM1 expression

The evolving view of thermogenic fat and its implications in cancer and metabolic diseases

Vascular Permeability in Diseases

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