| Literature DB >> 32814756 |
Eriko Hisamatsu1, Manabu Nagao2, Ryuji Toh2, Yasuhiro Irino3, Takuya Iino3, Tetsuya Hara1, Hidekazu Tanaka1, Seimi Satomi-Kobayashi1, Tatsuro Ishida1, Ken-Ichi Hirata1,2.
Abstract
A large amount of evidence suggests that high-density lipoprotein (HDL) has anti-atherosclerotic properties. HDL-cholesterol (HDL-C) has also been widely used as a marker of cardiovascular disease. Recently, it was reported that plasma HDL-C levels are inversely correlated with cancer risk. However, the relationship between HDL and cancer pathophysiology remains unknown. Here, we sought to investigate the effect of HDL on cancer progression. First, we focused on fibronectin-an essential extracellular matrix glycoprotein-as an HDL-associated protein and found that only 7.4% of subjects in this study had fibronectin in HDL isolated from their plasma. The fibronectin-containing HDL (FN-HDL) increased the phosphorylation of focal adhesion kinase (FAK) in HeLa cells compared to HDL without fibronectin, further inducing the phosphorylation in a dose-dependent manner. Second, we found that fibronectin-treated HDL activated the phosphorylation of FAK, and its upstream effector blocked the phosphorylation induced by FN-HDL. Finally, we demonstrated that FN-HDL promoted cancer cell proliferation and adhesion compared to HDL without fibronectin. Our study showed the possible mechanism by which FN-HDL enhanced cancer cell proliferation and adhesion via the FAK signaling pathway. Further investigation of the roles of HDL components in tumorigenesis might provide novel insight into cancer pathophysiology.Entities:
Keywords: Cancer progression; Fibronectin; Focal Adhesion Kinase; High-density lipoprotein
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Year: 2020 PMID: 32814756 PMCID: PMC7447102
Source DB: PubMed Journal: Kobe J Med Sci ISSN: 0023-2513