Open AccessTRIP13 is expressed in colorectal cancer and promotes cancer cell invasion
Author(s) -
Kenji Kurita,
Masao Maeda,
Mohammed Mansour,
Toshio Kokuryo,
K. Uehara,
Yukihiro Yokoyama,
Masato Nagino,
Michinari Hamaguchi,
Takeshi Senga
Publication year - 2016
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5332
Subject(s) - oncogene , cancer , cell cycle , cancer research , cell growth , colorectal cancer , biology , cell , genetics
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.