Abstract Caveolin-1 (Cav-1) is an important component of the protein of the nest structure. It is essentially an internal insulation of the membrane and is involved in various cell processes, including internal osmosis, cholesterol distribution, cell transport and signal transmission. Over the past 10-15 years, there has been growing evidence that Cav-1 plays an important role in diseases such as cancer, diabetes and fibrosis. Cav-1 plays a positive and negative role in different diseases through different regulatory approaches. Here, we review the current literature on Cav-1 in different diseases and discuss the role of Cav-1 in human organs and diseases.
Key words Caveolin-1; cancer; disease; organ function
The prefaces Yamada and Palade began their study of the nest as early as 1955 [1]. The term “caveolae” means “small dents” or “small caves” and is used to describe the bottling membranes [2] observed in upper skin cells. Peaks are different from other membrane rafts, mainly because of the presence of surface-marked proteins (feedhead proteins) that interact with cholesterol. In addition, Caveolin plays an important role in cell separation, development, migration, inflammation, stress and immunization. The Caveolin family consists of three members: Caveolin-1 (Cav-1), Caveolin-2 (Cav-2) and Caveolin-3 (Cav-3) [3]. Cav-1 is the most important structural component of the nest, which interacts with the cell skeleton inside the cell and with the external ecular matrix (ECM) of the cell and is usually considered the main regulating factor for cell signal transmission [4]. In recent years, Cav-1 has been found to express abnormally in a variety of diseases, including cancer, sclerosis of anorexia and muscular malnutrition [5]. This overview presents the molecular characteristics and functions of Cav-1 and its relationship to disease.
Cav-1 and breast cancer are the most diagnosed cancers among women and have become the leading causes of cancer-related mortality and disability [25]. The human Cav-1 gene map shows a suspected tumour inhibition genetic position (D7S522/7/q31.1), often missing in human breast cancer. A growing number of experimental studies have shown that Cav-1 plays a key role in the progress of breast cancer, including cell proliferation, death, self-absorption, invasion, migration and transfer. Cav-1 can be used as a tumour inhibitor in MCF-7 cells; the downward revision of Cav-1 promotes proliferation by increasing the expression and function of the Membrane Large Electrolytic Ca2+ Activated Potassium (BKCa) channel, thereby promoting the occurrence of malignant tumours and thus accelerating the process of cancer[26]. Importantly, the reduction and self-absorption levels of Cav-1 were observed in human breast cancer cells and tissue[27]. Following the chemical analysis of Cav-1 and EGR of 306 patients using immunochemicals, Liang et al.[28] found that the Cav-1 matrix had tumor inhibition, while the material Cav-1 expression promoted EGR signaling in breast cancer, which may be necessary for the filamental start of the EGFR medium. Another study reported that IM Cav-1 expression was an independent pre-posterative factor for breast cancer, and that the absence or decrease of Cav-1 expression in IMECAF presaged poor prognosis.[29] The acidization of the Cav-1 in the Tyr14 residual was essential for the de-stabilization of Cav-1, which led to a significantly lower expression of Cav-1 in the tumour ball than in the tumour cell [30]. Further studies [31] indicate that aerobic fermentation of breast cancer cells can be inhibited by regulating the Cav-1/NF-100B/c-Myc route. In contrast, the Cav-1 expression is associated with tumour malignant progress, as Akt1 can phosphate RhoC GTPase [32] by activation of an inflammating breast cancer cell attack with Akt1. In addition, Cav-1 can inhibit the death of human breast cancer cells [33].
