Tumor angiogenesis and anti-angiogenic therapies

Shahneh, Fatemeh Zare; Baradaran, Behzad; Zamani, Fatemeh; Aghebati‐Maleki, Leili

doi:10.3233/hab-130267

Cited by 71 publications

(52 citation statements)

References 57 publications

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“…The VEGF family comprises from VEGF (VEGF-A), VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PGF), which have been reported to be the key regulators of tumor-angiogenesis [23][24][25]. No significant alterations in VEGF-C, VEGF-B, VEGF-D and PGF expression were observed (data not shown).…”

Section: Depletion Of Sult2b1b In Gc Cells Reduces Vegf-a Expression mentioning

confidence: 81%

Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

Chen

Zhou

et al. 2016

Cell Physiol Biochem

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Background/Aims: Overexpression of cytosolic sulfotransferase 2B1b (SULT2B1b) has been commonly found in colorectal and hepatocellular carcinoma, suggesting that SULT2B1b might act as a potential oncogenic protein. However, its clinical significance and biological role in gastric cancer progression remain largely unknown. Methods: Expressions of SULT2B1b in clinical gastric cancer (GC) samples were examined using qRT-PCR and Western blot. Results: SULT2B1b was markedly overexpressed in human GC samples, and positively correlated with vessel density and associated with poor clinical features. We also demonstrated that overexpression of SULT2B1b resulted in increased tumor angiogenesis and tumor growth in mouse GC models. In addition, ablation of SULT2B1b in human GC cells lines BGC823 and MKN45 decreased the capability of the cells to recruit endothelial cells. Moreover, depletion of SULT2B1b in GC cells reduced VEGF-A expression by downregulating SP1 and AP2. Conclusion: Our results suggested that the SULT2B1b-mediated angiogenic pathway could serve as biomarkers for GC diagnosis and prognosis, and suppressing SULT2B1b-mediated angiogenic signaling might be a promising strategy for developing novel GC treatment.

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Section: Depletion Of Sult2b1b In Gc Cells Reduces Vegf-a Expression mentioning

confidence: 81%

Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

Chen

Zhou

et al. 2016

Cell Physiol Biochem

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“…Proces nowotworzenia aktywuje angiogenezę, tworząc ciągle rozrastającą się sieć naczyń w wyniku tzw. pączkowa-nia (sprouting angiogenesis) komórek śródbłonka ścian i końców naczyń włosowatych [17], co pozwala na rozrost i odżywianie się guza [18]. Naczynia krwionośne wytworzone wewnątrz guzów w wyniku ciągłej angiogenezy różnią się od naczyń tkanek prawidło-wych [19].…”

Section: Inicjowanie Procesu Angiogenezyunclassified

“…New blood vessels transform into functional arteries, while new blood vessels are also formed from already existing ones, both in the process of arteriogenesis. The process of neoplasia activates angiogenesis, creating an ever-expanding vascular network as a result of so-called sprouting angiogenesis of endothelial cells and capillary ends [17], which enables tumour growth and nourishment [18]. The blood vessels created inside tumours as a result of continuous angiogenesis differ from normal tissue vessels [19].…”

Section: Initiation Of Angiogenesismentioning

confidence: 99%

Molecular mechanisms of neoplasia

Derkacz

Komosińska-Vassev

2017

Ann. Acad. Med. Siles.

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The evolution of normal cells into neoplastic cells involves many stages. This paper describes six characteristics of tumour cells: maintenance of cell division-promoting signals, resistance to exogenous growth inhibitors, avoidance of apoptosis, acquisition of the ability to undergo an infinite number of divisions, induction of angiogenesis as well as activation of the ability to invade and metastasise. The listed and described characteristics of tumor cells are associated with genomic instability and the production of inflammation. Genomic instability protes the formation of a diverse pool of cells, and the accumulation of traits of tumor cells leads to inflammation. The progress of science has enabled the addition of two further features acquired by cells during the process of neoplasia -modification of cellular metabolism and avoidance of recognition by the immune system. K E Y W O R D Sangiogenesis, apoptosis, genomic instability, neoplastic progression ST R ES ZCZ E NI EEwolucja komórki prawidłowej w nowotworową obejmuje wiele etapów. W pracy opisano sześć cech charakteryzują-cych komórki nowotworowe: utrzymanie sygnałów stymulujących podziały komórkowe, oporność na egzogenne inhibitory wzrostu, unikanie apoptozy, nabywanie zdolności do nieskończonej liczby podziałów, indukcję angiogenezy oraz aktywację zdolności do inwazji i przerzutowania. U podłoża wymienionych cech leży nie tylko niestabilność genomu promująca wytworzenie zróżnicowanej genetycznie puli komórek, ale także stan zapalny, który wymaga wystąpienia wielu cech charakterystycznych dla komórek nowotworowych. Postęp badań pozwolił dodać dwie kolejne cechy nabyte przez komórki w czasie nowotworzenia -modyfikację metabolizmu komórkowego oraz unikanie rozpoznania przez system immunologiczny.

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“…The vascular endothelial growth factor (VEGF) family, including VEGF-A, -B,-C, -D and placental growth factor (PlGF), play an essential role in activating quiescent endothelial cells and promoting cell proliferation, migration and vascular permeability. VEGF-A is the first and the most well studied member of the VEGF family and currently viewed as a key target for anti-angiogenic therapy [7].…”

Section: Introductionmentioning

confidence: 99%