2020: Lok and co. discovered that weakening of the spindle-assembly checkpoint is a mechanism underlying mitotic slippage. As mitotic slippage is critical for both cancer development and effectiveness of a major class of cancer therapies, these new findings extend our fundamental understanding of how cancer cells develop in the first place and subsequently respond to therapies.
Lok TS, Wang Y, Xu WK, Xie S, Ma HT, and Poon RYC (2020) Mitotic slippage is determined by p31comet and the weakening of the spindle-assembly checkpoint. Oncogene 39: 2819-34.
2020: Joyce Mak demonstrated that inactivation of ATM acts synergistically with PARP1 inhibitors in promoting cell death in cancer cells. This study implies that ATM is an important anti-cancer target for therapies using PARP inhibitors.
Mak JPY, Ma HT and Poon RYC (2020) Synergism between ATM and PARP1 inhibition involves DNA damage and abrogating the G2 DNA damage checkpoint. Molecular Cancer Therapeutics 19: 123-134.
30 May 2019
2nd Workshop on Mitotic Fidelity, HKUST.
Organizer: R.Y.C. Poon
Speakers: Franco Au (HKUST), Gary Chan (HKU), William Chao (U Macau), Yick Hin Ling (HKU), Ken Ma (HKUST)
2019: a superior conditional KO system generated using CRISPR-Cas9 and rescue constructs under the control of Tet promoter and AID degron. Great for studying essential genes.
Vectors described in the paper can be obtained from Addgene.
Ng LY, Ma HT, Liu JCY, Huang X, Lee N, and Poon RYC (2019) Conditional gene inactivation by combining tetracycline-mediated transcriptional repression and auxin-inducible degron-mediated degradation. Cell Cycle 18: 238-48.
2019: Zeng and co. addressed an important issue in anti-cancer drug responses. They found that mitotic slippage prevents mitotic cell death caused by spindle poisons but reduces subsequent long term survival. The specific temporal patterns of cell death may reconcile the contradictory results from many previous studies.
Zeng X, Xu WK, Lok TM, Ma HT, and Poon RYC (2019) Imbalance of the spindle-assembly checkpoint promotes spindle poison-mediated cytotoxicity with distinct kinetics. Cell Death and Disease 10: 314.
2018: Ken Ma published a complementary paper to our 2016 study on TRIP13. This new study finally explains the paradox of why TRIP13 is required for the activation of the spindle-assembly checkpoint (in addition to its role in inactivating the checkpoint).
Ma HT and Poon RYC (2018) TRIP13 functions in the establishment of the spindle-assembly checkpoint by replenishing O-MAD2. Cell Reports 22: 1439-50.
Ma HT and Poon RYC (2016) TRIP13 regulates both the activation and inactivation of the spindle-assembly checkpoint. Cell Reports 14: 1086-99.