PTRF is associated with caveolin 1 at the time of receptivity: but SDPR is absent at the same time

Abstract

The plasma membrane of uterine epithelial cells undergoes a number of changes during early pregnancy. The changes in the basolateral membrane at the time of implantation in particular change from being smooth to highly tortuous in morphology, along with a dramatic increase in the number of morphological caveolae at this time. The major protein of caveolar membranes is caveolin, and previous studies have shown that RNA pol I transcription factor (PTRF) and serum deprivation protein response (SDPR) are the two members of the cavin protein family. These proteins are known to be involved in caveolae biogenesis, where they directly bind to cholesterol and lipids and have been reported to promote membrane curvature. As there is an increase in membrane tortuosity and caveolae at the time of implantation, this study investigated PTRF and SDPR to explore the possible roles that they play in the morphology of the uterine epithelium during early pregnancy. PTRF protein abundance did not change in uterine epithelial cells during early pregnancy or in response to ovarian hormones. At the time of implantation in uterine epithelial cells, PTRF co-immunoprecipitated with caveolin 1, thereby demonstrating an association with caveolin-1 at the basal plasma membrane in caveolae. SDPR protein was observed to be present only at the time of fertilisation, and also under the influence of oestrogen alone, where a cytoplasmic localisation in uterine epithelial cells was observed. The localisation and expression PTRF and SDPR in uterine epithelial cells during early pregnancy suggest that they have roles in the maintenance of lipids and cholesterol in the plasma membrane. PTRF and lack of SDPR may contribute not only to the morphology of the basal plasma membrane as observed at the time of implantation, but also to the maintenance of epithelial polarity during early pregnancy.

Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor‐β signaling

“…(15,16) Lack of SDPR contributes not only to the morphology of the basal plasma membrane, but also to the maintenance of epithelial polarity during early pregnancy. (17) In our study, we found that SDPR decreases EMT programs in human breast cancer cells, including upregulation of epithelial markers (E-cadherin and b-catenin) and downregulation of mesenchymal markers (Vimentin and N-cadherin). These findings demonstrated that SDPR inhibits EMT phenotype in breast cancer cells.…”

“…During EMT, epithelial cells lose their cell polarity and molecular expression, enabling cell–cell adhesion, and they gain migratory and invasive properties . Lack of SDPR contributes not only to the morphology of the basal plasma membrane, but also to the maintenance of epithelial polarity during early pregnancy . In our study, we found that SDPR decreases EMT programs in human breast cancer cells, including upregulation of epithelial markers (E‐cadherin and β‐catenin) and downregulation of mesenchymal markers (Vimentin and N‐cadherin).…”