PDF(Pubmed)
Abstract：
Plakophilin 3 (PKP3), a component of desmosome, is aberrantly expressed in many kinds of human diseases, especially in cancers. Through direct interaction, PKP3 binds with a series of desmosomal proteins, such as desmoglein, desmocollin, plakoglobin, and desmoplakin, to initiate desmosome aggregation, then promotes its stability. As PKP3 is mostly expressed in the skin, loss of PKP3 promotes the development of several skin diseases, such as paraneoplastic pemphigus, pemphigus vulgaris, and hypertrophic scar. Moreover, accumulated clinical data indicate that PKP3 dysregulates in diverse cancers, including breast, ovarian, colon, and lung cancers. Numerous lines of evidence have shown that PKP3 plays important roles in multiple cellular processes during cancer progression, including metastasis, invasion, tumor formation, autophagy, and proliferation. This review examines the diverse functions of PKP3 in regulating tumor formation and development in various types of cancers and summarizes its detailed mechanisms in the occurrence of skin diseases.
摘要：
斑素3(PKP3),桥粒的一个组成部分，在许多人类疾病中异常表达，尤其是在癌症中。通过直接互动,PKP3与一系列桥粒蛋白结合，比如desmoglein，desmocollin,血红蛋白,和desmoplakin，为了启动桥粒聚集，促进其稳定性。由于PKP3主要在皮肤中表达，PKP3的丢失促进了几种皮肤病的发展，比如副肿瘤性天疱疮，寻常型天疱疮,和肥厚性瘢痕.此外，积累的临床数据表明，PKP3在多种癌症中失调，包括乳房,卵巢,结肠,和肺癌。许多证据表明，PKP3在癌症进展过程中的多个细胞过程中发挥重要作用。包括转移,入侵,肿瘤形成，自噬,和扩散。本文综述了PKP3在各种类型癌症中调节肿瘤形成和发展的多种功能，并总结了其在皮肤病发生中的详细机制。
