Abstract
Vasohibin-1 (VASH1) is an endogenous angiogenesis inhibitor.However, the clinical relevance of VASH1 in colon cancer and its regulations on cancer angiogenesis and cancer cell biological characteristics are still unknown. Here we showed that stromal VASH1 levels were negatively correlated with tumor size, advanced clinical stage and distant metastases in colon cancer patients. Overexpression of VASH1 in colon cancer cells induced apoptosis and senescence, inhibiting cancer cell growth and colony formation in vitro and tumor growth in vivo. In addition, knockdown of VASH1 in cancer cells promoted cell growth, adhesion and migration in vitro, and enhanced tumorigenesis and metastasis in vivo.
Highlights
IntroductionThere are 100, 000 new cases of colon cancer and 50, 000 cases estimated deaths a year [1, 2]
Colorectal cancer (CRC) is a major cause of cancer death in the USA and worldwide
Our results collectively suggest that both active angiogenesis and lymphoangiogenesis exist in colon cancer patients, and that VASH1 is prevalent in the cancer stroma of cancer tissues
Summary
There are 100, 000 new cases of colon cancer and 50, 000 cases estimated deaths a year [1, 2]. Understanding the pathogenesis and regulatory processes during cancer development will provide novel strategies for colon cancer treatment. In addition to the genetically controlled development of tumor cells, tumor microenvironmental factors, such as tumor angiogenesis, are critical in enabling tumor growth, progression and distant metastasis [3]. Homeostasis of tumor angiogenesis is controlled by a panel of angiogenesis stimulators and inhibitors expressed in tumor cells and stroma cells in the tumor microenvironment [3,4,5,6,7]. A better understanding of biological functions and regulations of those stimulators and inhibitors will provide novel targets for the effective antiangiogenic therapy against colon cancer and other cancers as well
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