Kurita Kenji, Maeda Masao, Mansour Mohammed A, Kokuryo Toshio, Uehara Keisuke, Yokoyama Yukihiro, Nagino Masato, Hamaguchi Michinari, Senga Takeshi
Department of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Division of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Oncol Lett. 2016 Dec;12(6):5240-5246. doi: 10.3892/ol.2016.5332. Epub 2016 Nov 1.
Thyroid hormone receptor interactor 13 (TRIP13) is a member of the ATPases associated with various cellular activities family of proteins and is highly conserved in a wide range of species. Recent studies have demonstrated that TRIP13 is critical for the inactivation of the spindle assembly checkpoint and is associated with the progression of certain cancers. In the present study, the role of TRIP13 in colorectal cancer (CRC) was examined. Reverse transcription-quantitative polymerase chain reaction analysis revealed that TRIP13 messenger RNA was highly expressed in multiple CRC tissues. The depletion of TRIP13 in CRC cells suppressed cell proliferation, migration and invasion. To determine whether the catalytic activity of TRIP13 was critical for cancer progression, an inactive mutant of TRIP13 was expressed in CRC cells. The invasion of cancer cells that expressed the mutant TRIP13 was significantly reduced compared with that of the wild type TRIP13-expressing cancer cells. These results indicate that TRIP13 could be a potential target for CRC treatment.
甲状腺激素受体相互作用蛋白13(TRIP13)是与各种细胞活动相关的ATP酶家族蛋白的成员,在广泛的物种中高度保守。最近的研究表明,TRIP13对纺锤体组装检查点的失活至关重要,并且与某些癌症的进展相关。在本研究中,检测了TRIP13在结直肠癌(CRC)中的作用。逆转录定量聚合酶链反应分析显示,TRIP13信使核糖核酸在多个CRC组织中高表达。CRC细胞中TRIP13的缺失抑制了细胞增殖、迁移和侵袭。为了确定TRIP13的催化活性对癌症进展是否至关重要,在CRC细胞中表达了TRIP13的无活性突变体。与表达野生型TRIP13的癌细胞相比,表达突变型TRIP13的癌细胞的侵袭明显减少。这些结果表明,TRIP13可能是CRC治疗的潜在靶点。