Pan Ze-Ya, Yang Yun, Pan Hao, Zhang Jin, Liu Hui, Yang Yuan, Huang Gang, Yin Lei, Huang Jian, Zhou Wei-Ping
The Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University Shanghai 200438, China.
Department of Infectious Disease Control and Prevention, Shanghai Municipal Center for Disease Control and Prevention 1380 West Zhongshan Road, Shanghai 200336, China.
Int J Clin Exp Med. 2015 Feb 15;8(2):2334-41. eCollection 2015.
Tumor protein D52-like 2, known as hD54 in previous studies (TPD52L2), is a member of TPD52 family which has been implicated in multiple human cancers. In recent reports, TPD52 proteins were indicated to be associated with several malignancies, but very little is known about the function of TPD52L2 in liver cancers. In our present study, in order to explore the role of TPD52L2 in liver cancer, TPD52L2 was knocked down in SMMC-7721 liver cancer cell line by lentivirus mediated RNA interference. The results demonstrated that depletion of TPD52L2 could remarkably inhibit proliferation and colony forming ability of cancer cell SMMC-7721. Furthermore, cell cycle in TPD52L2 depleted cells was verified to be arrested in G0/G1 phase as determined by FACS assay, in consistence with the observation of cell proliferation inhibition. These results unraveled that TPD52L2 played an important role in tumorigenesis pathways of liver cancer and might serve as a promising target in human liver cancer diagnosis and therapy.
肿瘤蛋白D52样蛋白2，在先前的研究中称为hD54（TPD52L2），是TPD52家族的成员，该家族与多种人类癌症有关。在最近的报道中，TPD52蛋白被指出与几种恶性肿瘤有关，但关于TPD52L2在肝癌中的功能却知之甚少。在我们目前的研究中，为了探索TPD52L2在肝癌中的作用，通过慢病毒介导的RNA干扰在SMMC-7721肝癌细胞系中敲低TPD52L2。结果表明，TPD52L2的缺失可显著抑制癌细胞SMMC-7721的增殖和集落形成能力。此外，通过流式细胞术分析证实，TPD52L2缺失细胞的细胞周期停滞在G0/G1期，这与细胞增殖抑制的观察结果一致。这些结果表明，TPD52L2在肝癌的肿瘤发生途径中起重要作用，可能成为人类肝癌诊断和治疗中有前景的靶点。
