Oshima R G, Baribault H, Caulín C
Burnham Institute, La Jolla, CA 92037, USA.
Cancer Metastasis Rev. 1996 Dec;15(4):445-71. doi: 10.1007/BF00054012.
Keratin 8 (K8) and keratin 18 (K18) are the most common and characteristic members of the large intermediate filament gene family expressed in 'simple' or single layer epithelial tissues of the body. Their persistent expression in tumor cells derived from these epithelia has led to the wide spread use of keratin monoclonal antibodies as aids in the detection and identification of carcinomas. Oncogenes which activate ras signal transduction pathways stimulate expression of the K18 gene through transcription factors including members of the AP-1 (jun and fos) and ETS families. The persistent expression of K8 and K18 may reflect the integrated transcriptional activation of such transcription factors and, in the cases of ectopic expression, an escape from the suppressive epigenetic mechanisms of DNA methylation and chromatin condensation. Comparison of the mechanisms of transcriptional control of K18 expression with expression patterns documented in both normal and pathological conditions leads to the proposal that persistent K8 and K18 expression is a reflection of the action of multiple different oncogenes converging on the nucleus through a limited number of transcription factors to then influence the expression of a large number of genes including these keratins. Furthermore, correlation of various tumor cell characteristics including invasive behavior and drug sensitivity with K8 and K18 expression has stimulated consideration of the possible functions of these proteins in both normal development and in tumorigenesis. Recent developments in the analysis of the functions of these intermediate filament proteins provide new insights into diverse functions influenced by K8 and K18.
角蛋白8(K8)和角蛋白18(K18)是在身体的“单层”或单层上皮组织中表达的大型中间丝基因家族中最常见且具有特征性的成员。它们在源自这些上皮组织的肿瘤细胞中持续表达,导致角蛋白单克隆抗体被广泛用于辅助检测和鉴定癌。激活ras信号转导途径的癌基因通过包括AP-1(jun和fos)和ETS家族成员在内的转录因子刺激K18基因的表达。K8和K18的持续表达可能反映了这些转录因子的整合转录激活,并且在异位表达的情况下,是从DNA甲基化和染色质浓缩的抑制性表观遗传机制中逃脱。将K18表达的转录控制机制与正常和病理条件下记录的表达模式进行比较,得出的结论是,K8和K18的持续表达反映了多种不同癌基因通过有限数量的转录因子汇聚到细胞核,进而影响包括这些角蛋白在内的大量基因表达的作用。此外,各种肿瘤细胞特征(包括侵袭行为和药物敏感性)与K8和K18表达的相关性,促使人们考虑这些蛋白质在正常发育和肿瘤发生中的可能功能。这些中间丝蛋白功能分析的最新进展为K8和K18影响的多种功能提供了新的见解。