Abstract
Sialomucin complex (SMC, rat Muc4) is a heterodimeric glycoprotein complex consisting of a mucin subunit ASGP-1 (Ascites sialoglycoprotein-1) and a transmembrane subunit ASGP-2, which is highly overexpressed on the surface of ascites 13762 rat mammary adenocarcinoma cells. The complex is produced from a single gene and polypeptide precursor. SMC is developmentally regulated in normal rat mammary gland by multiple and complex mechanisms, with levels in the lactating gland being 100-fold those in the virgin gland. SMC transcript levels are enhanced in normal rat mammary epithelial cells by fetal bovine serum, insulin, and IGF-1 by an ERK-1/2-dependent pathway. SMC is post-transcriptionally regulated by Matrigel (extracellular matrix) by inhibition of SMC precursor synthesis. SMC is also post-transcriptionally regulated by TGF-β by disruption of SMC precursor processing into mature ASGP-1 and ASGP-2. The inhibition of SMC levels by TGF-β occurs by an ERK1/2-independent pathway, suggesting that the SMAD or another pathway may be involved in this effect. Interestingly, the inhibition of SMC levels by TGF-β can be blocked by treatment with IFN-γ, which has been shown to block TGF-β effects via a Jak/Stat-dependent pathway. This effect is dose-responsive and is dependent on the order in which the cytokines are added, suggesting that the balance of signaling inputs is important in determining the expression level of SMC. Thus, SMC is regulated by multiple mechanisms, and the delicate interplay of the pathways involved serves to maintain normal levels of the complex and repress potential deleterious effects of overexpression.
Highlights
Lymph node biopsy is important as a prognostic factor, and influences therapy
In this study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis
This study was undertaken to determine the effect of wound healing drainages and postsurgical sera obtained from breast carcinoma (BC) patients on proliferation of dormant BC cells and to assess the role of HER2 oncoprotein in this proliferation
Summary
Lymph node biopsy is important as a prognostic factor, and influences therapy. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma, the net growth of epithelial cells results from a growth imbalance in favour of proliferation. The objective of this study was to assess the efficacy of hyperbaric oxygen therapy in symptomatic patients after breast cancer treatment. Conclusion: Hyperbaric oxygen therapy should be considered as a treatment option for patients with persisting symptomatology following breast-conserving therapy. We hypothesized that COX-2 expression was associated with that of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) in human breast cancer. Conclusion: COX-2 expression is significantly associated with increased cellular proliferation and angiogenesis in invasive breast cancer. Recent studies have demonstrated that the sentinel node biopsy (SNB) is a reliable and minimally invasive method for determining the axillary node status in patients with breast cancer. Conclusion: Overexpression of episialin strongly inhibits fat secretion, and critically affects timing of involution of the lactating mammary gland
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