The role of VEGF in the diagnosis and treatment of malignant pleural effusion in patients with non‑small cell lung cancer (Review)

Abstract

Malignant pleural effusion (MPE) is a severe medical condition, which can result in breathlessness, pain, cachexia and reduced physical activity. It can occur in almost all types of malignant tumors; however, lung cancer is the most common cause of MPE, accounting for ~1/3 of clinical cases. Although there are numerous therapeutic approaches currently available for the treatment of MPE, none are fully effective and the majority can only alleviate the symptoms of the patients. Vascular endothelial growth factor (VEGF) has now been recognized as one of the most important regulatory factors in tumor angiogenesis, which participates in the entire process of tumor growth through its function to stimulate tumor angiogenesis, activate host vascular endothelial cells and promote malignant proliferation. Novel drugs targeting VEGF, including endostar and bevacizumab, have been developed and approved for the treatment of various tumors. Data from recent clinical studies have demonstrated that drugs targeting VEGF are effective and safe for the clinical management of MPE. Therefore, VEGF-targeting represents a promising novel strategy for the diagnosis and treatment of MPE. The present review summarized recent advances in the role of VEGF in the pathogenesis, diagnosis and clinical management of MPE in patients with non-small cell lung cancer.

Malignant Pleural Effusion and Its Current Management: A Review

“…The effects of these can be divided into three categories: The first group of molecules stimulate the pleural inflammation (e.g., interleukin 2—IL2; tumor necrosis factor—TNF and interferon—INF); the second group of molecules stimulate tumor angiogenesis (e.g., angiopoietin 1 (ANG-1), angiopoietin 2 (AGN–2); the third group of molecules affect vascular hyperpermeability (e.g., vascular endothelial growth factor—VEGF, matrix metalloproteinases—MMP, chemokine (c-c motif) ligand 2—CCL, osteopontin—OPN, etc.) [1,19]. Additionally, studies show that mastocytes have a significant effect on MPE formation.…”

“…In the last decade, researchers used genome analysis of tumor cells and discovered that tumors which have activating mutations EGFR , KRAS , PIK3CA , BRAF , MET , EML4/ALK and RET are connected to increased MPE formation [18,19,21]. KRAS mutations are common for distant metastases and EGFR mutations for tumors which metastasize via direct infiltration [18].…”

Effect of bevacizumab against cystic components of brain tumors

“…Marked elevation of VEGF was also reported in both malignant pleural effusion and malignant ascites, and considered to be a key molecule . Both malignant pleural effusion and malignant ascites were poor prognostic factor and resulted in decline of quality of life (QOL) . Bevacizumab combined with chemotherapy were reported to be a superior option for patients with both malignant pleural effusion and malignant ascites, and could improve patients' QOL .…”

Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer Based on network pharmacology and molecular docking

“…Fucosterol can directly activate the Ras signaling pathway, PI3K-Akt signaling pathway, and ErbB signaling pathway, and indirectly activate the MAPK signaling pathway to regulate cell proliferation and apoptosis to achieve the therapeutic effect on NSCLC. From the perspective of the key signal transduction pathways( Figure 8B), it was found that both VEGF signaling pathway and ErbB signaling pathway can activate downstream signals to control angiogenesis, affect cell proliferation and migration, and play a crucial role in the development and metastasis of tumors [37][38][39]. Meanwhile, the PI3K-Akt signaling pathway participates in the regulation of cell cycle progression [40][41][42].…”