Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University, School of Medicine, 751 N Rutledge St. PO Box 19626, Springfield, IL 627794-9626, USA.
Front Biosci (Landmark Ed). 2010 Jan 1;15(1):226-36. doi: 10.2741/3617.
Myoepithelial cells form a semi-continuous protective sheet separating the human breast epithelium and the surrounding stroma. They suppress stromal invasion of tumor cells by the secretion of various anti-angiogenic and anti-invasive factors. The disruption of this cell layer results in the release of the growth factors, angiogenic factors, and reactive oxygen species causing an alteration in the microenvironment. This helps in the proliferation of surrounding cells and increases the invasiveness of tumor cells. Two theories are proposed for the mechanism of tumor epithelial cells progression from in situ to invasive stage. According to the first theory, tumor cell invasion is triggered by the overproduction of proteolytic enzymes by myoepithelial cells and surrounding tumor cells. The second theory states that tumor invasion is a multistep process, the interactions between damaged myoepithelial cells and the immunoreactive cells trigger the release of basement membrane degrading enzymes causing tumor progression. Further studies in understanding of molecular mechanism of myoepithelial cell functions in tumor suppression may lead to the identification of novel therapeutic targets for breast cancer.
肌上皮细胞形成半连续的保护层,将人乳腺上皮细胞与周围基质分开。它们通过分泌各种抗血管生成和抗侵袭因子来抑制肿瘤细胞向基质的浸润。这种细胞层的破坏导致生长因子、血管生成因子和活性氧的释放,从而改变微环境。这有助于周围细胞的增殖,并增加肿瘤细胞的侵袭性。有两种理论被提出用于解释肿瘤上皮细胞从原位到侵袭阶段的进展机制。根据第一个理论,肿瘤细胞的浸润是由肌上皮细胞和周围肿瘤细胞过度产生蛋白水解酶触发的。第二个理论指出,肿瘤浸润是一个多步骤的过程,受损的肌上皮细胞与免疫反应细胞之间的相互作用触发基底膜降解酶的释放,导致肿瘤进展。进一步研究肌上皮细胞在肿瘤抑制中的功能的分子机制,可能会发现乳腺癌的新治疗靶点。