Jin Fu Kang Oral Liquid Inhibits Lymphatic Endothelial Cells Formation and Migration.

Hai-Lang He,Dan Wang,Xian-Mei Zhou,Jian-Xin Li,Jie Tang,Ling Xu

doi:10.1155/2016/3635209

Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide. Jin Fu Kang (JFK), an oral liquid prescription of Chinese herbal drugs, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). Lymphangiogenesis is a primary event in the process of cancer development and metastasis, and the formation and migration of lymphatic endothelial cells (LECs) play a key role in the lymphangiogenesis. To assess the activity of stromal cell-derived factor-1 (SDF-1) and the coeffect of SDF-1 and vascular endothelial growth factor-C (VEGF-C) on the formation and migration of LECs and clarify the inhibitory effects of JFK on the LECs, the LECs were differentiated from CD34+/VEGFR-3+ endothelial progenitor cells (EPCs), and JFK-containing serums were prepared from rats. SDF-1 and VEGF-C both induced the differentiation of CD34+/VEGFR-3+ EPCs towards LECs and enhanced the LECs migration. Couse of SDF-1 and VEGF-C displayed an additive effect on the LECs formation but not on their migration. JFK inhibited the formation and migration of LECs, and the inhibitory effects were most probably via regulation of the SDF-1/CXCR4 and VEGF-C/VEGFR-3 axes. The current finding suggested that JFK might inhibit NSCLC through antilymphangiogenesis and also provided a potential to discover antilymphangiogenesis agents from natural resources.

Highlights

Lung cancer, as the leading cause of cancer-related deaths worldwide, is the most common cancer affecting both men and women and holds approximately 27% of all cancer deaths in the United States [1]
Our results clearly demonstrated that stromal cell-derived factor-1 (SDF-1) and vascular endothelial growth factor-C (VEGF-C) promoted the CD34+/VEGFR-3+ endothelial progenitor cells (EPCs) to differentiate to the lymphatic endothelial cells (LECs) that showed positive lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) staining, a specific LEC marker, and enhanced the LECs migration
This study demonstrated that SDF-1 and VEGF-C induced CD34+/VEGFR-3+ EPCs to differentiate towards LECs and enhanced the LECs migration

Summary

Introduction

As the leading cause of cancer-related deaths worldwide, is the most common cancer affecting both men and women and holds approximately 27% of all cancer deaths in the United States [1]. The cancer cell migration to distant tissues occurs through blood and lymphatic vessels and is essential for tumor growth and metastasis [3]. Cancer metastasis is a very important event in cancer development and accounts for approximately 90% of treatment failure and related deaths for all cancer. Lymphatic metastasis to regional lymph nodes has been focused on as a major indicator for the staging and the prognosis of most human cancers, and accurate lymph node staging is one of the most important factors in the NSCLC treatment and prognosis [4]. Growing evidences revealed that the lymphatic vasculature and tumors interact with each other and promote metastasis formation [5]. Lymphatic metastasis closely relates to the tumor-induced formation and growth of new lymphatic vessels, named as lymphangiogenesis, an important initial event in tumor growth and spread

Methods

Discussion

Conclusion