Role of von Willebrand factor in the angiogenesis of lung adenocarcinoma

Lung adenocarcinoma (LUAD) has a high morbidity and mortality rate worldwide, and its growth and metastasis require angiogenesis. The density of microvessels in LUAD is positively correlated with metastasis and recurrence. Von Willebrand factor (VWF) is a multifunctional glycoprotein in blood plasma. Recent evidence shows that VWF inhibits angiogenesis through regulation of angiopoietin-2 (Ang-2) and integrin alpha v beta 3. LUAD patients exhibit an increase in the plasma VWF/ADAMTS-13 ratio. Gene expression profiles of LUAD tissues indicate that VWF is differentially expressed in LUAD tissues compared to normal tissues. GATA binding protein 3 (GATA3) transcription factor may mediate VWF expression in LUAD. In this review, we summarize the role of VWF in LUAD and its regulatory mechanisms. We also discuss the potential of VWF as a diagnostic indicator and therapeutic target of LUAD.

Automated summary

Lung adenocarcinoma (LUAD) is a highly prevalent and deadly disease globally, and its growth and metastasis rely on angiogenesis. Recent evidence suggests that Von Willebrand factor (VWF) inhibits angiogenesis through regulation of angiopoietin-2 and integrin alpha v beta 3. LUAD patients exhibit an increased plasma VWF/ADAMTS-13 ratio, indicating the potential of VWF as a diagnostic indicator and therapeutic target for LUAD.