Wu Jing, Yang Rui, Ge Haize, Zhu Yu, Liu Shuye
Clinical Laboratory, Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Tianjin Institute of Hepatobiliary Disease, Artificial Cell Engineering Technology Research Center, The Third Central Hospital of Tianjin, Tianjin 300170, P.R. China.
Department of Genetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, P.R. China.
Exp Ther Med. 2024 Feb 1;27(3):124. doi: 10.3892/etm.2024.12412. eCollection 2024 Mar.
Breast cancer (BC) is the most commonly diagnosed cancer in women, providing a leading cause of death from malignancy. Pentraxin 3 (PTX3) and protein kinase C ζ (PKCζ) are both known to exert important roles in the progression of multiple types of tumors, including BC. The present study aimed to explore both their interaction and their role in promoting the proliferation and metastasis of BC. The expression level of PTX3 was found to be elevated both in patients with BC and in BC cells; furthermore, it was found to be associated with lymph node metastasis in patients with BC. Knockdown of PTX3 decreased the rate of cell proliferation and the effects of a series of metastasis-associated cellular processes, including cell chemotaxis, migration, adhesion and invasion, as well as diminishing actin polymerization of the MDA-MB-231 and MCF7 BC cells, and decreasing tumor pulmonary metastasis . Mechanistically, PTX3 and PKCζ were found to be colocalized intracellularly, and they were co-translocated to the cell membrane upon stimulation with epidermal growth factor. Following the knockdown of PTX3, both the phosphorylation and membrane translocation of PKCζ were significantly impaired, suggesting that PTX3 regulates the activation of PKCζ. Taken together, the findings of the present study have shown that PTX3 may promote the proliferation and metastasis of BC cells through regulating PKCζ activation to enhance cell migration, cell chemotaxis, cell invasion and cell adhesion.
乳腺癌（BC）是女性中最常被诊断出的癌症，是恶性肿瘤致死的主要原因。已知五聚体3（PTX3）和蛋白激酶Cζ（PKCζ）在包括BC在内的多种肿瘤进展中发挥重要作用。本研究旨在探讨它们之间的相互作用以及在促进BC增殖和转移中的作用。研究发现，PTX3在BC患者和BC细胞中的表达水平均升高；此外，还发现它与BC患者的淋巴结转移有关。敲低PTX3可降低细胞增殖率以及一系列与转移相关的细胞过程的效应，包括细胞趋化性、迁移、黏附和侵袭，同时减少MDA-MB-231和MCF7 BC细胞的肌动蛋白聚合，并减少肿瘤肺转移。从机制上讲，发现PTX3和PKCζ在细胞内共定位，并且在用表皮生长因子刺激后它们共同转位到细胞膜。PTX3敲低后，PKCζ的磷酸化和膜转位均受到显著损害，表明PTX3调节PKCζ的激活。综上所述，本研究结果表明，PTX3可能通过调节PKCζ激活来促进BC细胞的增殖和转移，从而增强细胞迁移、细胞趋化性、细胞侵袭和细胞黏附。
