State Key Laboratory of Genetic Engineering, Institute of Genetics, Fudan University, Shanghai 200433, PR China.
State Key Laboratory of Genetic Engineering, Institute of Genetics, Fudan University, Shanghai 200433, PR China; Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, PR China.
Biochem Biophys Res Commun. 2014 Mar 28;446(1):61-7. doi: 10.1016/j.bbrc.2014.02.049. Epub 2014 Feb 21.
TCP10L (T-complex 10 (mouse)-like) has been identified as a liver and testis-specific gene. Although a potential transcriptional suppression function of TCP10L has been reported previously, biological function of this gene still remains largely elusive. In this study, we reported for the first time that TCP10L was significantly down-regulated in clinical hepatocellular carcinoma (HCC) samples when compared to the corresponding non-tumorous liver tissues. Furthermore, TCP10L expression was highly correlated with advanced cases exceeding the Milan criteria. Overexpression of TCP10L in HCC cells suppressed colony formation, inhibited cell cycle progression through G0/G1 phase, and attenuated cell growth in vivo. Consistently, silencing of TCP10L promoted cell cycle progression and cell growth. Therefore, our study has revealed a novel suppressor role of TCP10L in HCC, by inhibiting proliferation of HCC cells, which may facilitate the diagnosis and molecular therapy in HCC.
TCP10L（与小鼠 T 复合体 10 同源）已被鉴定为肝脏和睾丸特异性基因。尽管之前已经报道了 TCP10L 具有潜在的转录抑制功能，但该基因的生物学功能仍很大程度上难以捉摸。在这项研究中，我们首次报道 TCP10L 在临床肝细胞癌（HCC）样本中与相应的非肿瘤性肝组织相比显著下调。此外，TCP10L 的表达与超过米兰标准的晚期病例高度相关。在 HCC 细胞中过表达 TCP10L 抑制集落形成，通过 G0/G1 期抑制细胞周期进程，并在体内减弱细胞生长。一致地，沉默 TCP10L 促进细胞周期进程和细胞生长。因此，我们的研究揭示了 TCP10L 在 HCC 中的新的抑制作用，通过抑制 HCC 细胞的增殖，这可能有助于 HCC 的诊断和分子治疗。
