Department of Colorectal Surgery, Beaumont Hospital, Dublin 9, Ireland.
Department of Physiology & Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 2, Ireland.
Cancer Metastasis Rev. 2019 Jun;38(1-2):237-257. doi: 10.1007/s10555-019-09781-w.
Overexpression of mucin glycoproteins has been demonstrated in many epithelial-derived cancers. The significance of this overexpression remains uncertain. The aim of this paper was to define the association of mucin glycoproteins with apoptosis, cell growth, invasion, migration, adhesion, and clonogenicity in vitro as well as tumor growth, tumorigenicity, and metastasis in vivo in epithelial-derived cancers by performing a systematic review of all published data. A systematic review of PubMed, Embase, and the Cochrane Central Register of Controlled Trials was performed to identify all papers that evaluated the association between mucin glycoproteins with apoptosis, cell growth, invasion, migration, adhesion, and clonogenicity in vitro as well as tumor growth, tumorigenicity, and metastasis in vivo in epithelial-derived cancers. PRISMA guidelines were adhered to. Results of individual studies were extracted and pooled together based on the organ in which the cancer was derived from. The initial search revealed 2031 papers, of which 90 were deemed eligible for inclusion in the study. The studies included details on MUC1, MUC2, MUC4, MUC5AC, MUC5B, MUC13, and MUC16. The majority of studies evaluated MUC1. MUC1 overexpression was consistently associated with resistance to apoptosis and resistance to chemotherapy. There was also evidence that overexpression of MUC2, MUC4, MUC5AC, MUC5B, MUC13, and MUC16 conferred resistance to apoptosis in epithelial-derived cancers. The overexpression of mucin glycoproteins is associated with resistance to apoptosis in numerous epithelial cancers. They cause resistance through diverse signaling pathways. Targeting the expression of mucin glycoproteins represents a potential therapeutic target in the treatment of epithelial-derived cancers.
黏蛋白糖蛋白在许多上皮来源的癌症中已有过表达的证明。这种过表达的意义尚不确定。本文的目的是通过对所有已发表的数据进行系统回顾，来定义黏蛋白糖蛋白与上皮来源的癌症中的细胞凋亡、细胞生长、侵袭、迁移、黏附和克隆形成体外以及肿瘤生长、致瘤性和转移的体内之间的关联。对 PubMed、Embase 和 Cochrane 对照试验中心注册库进行了系统的文献回顾，以确定所有评估黏蛋白糖蛋白与细胞凋亡、细胞生长、侵袭、迁移、黏附和克隆形成体外以及肿瘤生长、致瘤性和转移的体内之间关联的论文上皮来源的癌症。遵守 PRISMA 指南。根据癌症来源于的器官，提取和汇总个别研究的结果。最初的搜索显示出 2031 篇论文，其中 90 篇被认为符合纳入研究的标准。这些研究详细介绍了 MUC1、MUC2、MUC4、MUC5AC、MUC5B、MUC13 和 MUC16。大多数研究都评估了 MUC1。MUC1 的过表达与抗凋亡和化疗耐药性一致。还有证据表明，MUC2、MUC4、MUC5AC、MUC5B、MUC13 和 MUC16 的过表达也赋予了上皮来源的癌症抗凋亡能力。黏蛋白糖蛋白的过表达与许多上皮癌中的抗凋亡有关。它们通过多种信号通路引起耐药性。靶向黏蛋白糖蛋白的表达代表了治疗上皮来源的癌症的潜在治疗靶点。
